Peri-Implant Soft Tissue Management: A Clinical Guide 3031455150, 9783031455155

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Peri-Implant Soft Tissue Management A Clinical Guide Mohamed Hassan Editor

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Peri-Implant Soft Tissue Management

Mohamed Hassan Editor

Peri-Implant Soft Tissue Management A Clinical Guide

Editor Mohamed Hassan Oral Medicine, Infection & Immunity Harvard Dental School Boston, MA, USA

ISBN 978-3-031-45515-5    ISBN 978-3-031-45516-2 (eBook) https://doi.org/10.1007/978-3-031-45516-2 © Springer Nature Switzerland AG 2023 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Paper in this product is recyclable

Contents

1

 Introduction: Dental Implants and Soft Tissues: Roles and Challenges��������������������������������������������������������������������������������������������������   1 Mohamed Hassan

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 Histology and Anatomy of Different Types of Oral Mucosa������������������   5 Abdelghany Hassan Abdelghany

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 The Role and Importance of Soft Tissues for Long-Term Success of Dental Implants������������������������������������������������������������������������  15 Y. Natalie Jeong

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 Soft Tissue Management During Different Stage of Surgical Placement of Dental Implants������������������������������������������������������������������  27 Mohamed Hassan

5

 Proper Oral Hygiene Measures to Maintain Healthy Soft Tissues Around Dental Implants����������������������������������������������������������������������������  59 Irene Kim, Kevin Lin, and Soo Woo Kim

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 Management of Common Soft Tissue Pathology Around Dental Implants������������������������������������������������������������������������������������������������������  73 Mansour Hamad Alaskar

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 Prosthetic Role in Peri-Implant Soft Tissue Management: Treatment Planning Phase������������������������������������������������������������������������  97 Mohamed Moataz Khamis

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 Prosthetic Role in Peri-implant Soft Tissue Management: Prosthetic Phase ���������������������������������������������������������������������������������������� 129 Mohamed Moataz Khamis

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 Occlusion and Peri-implant Soft Tissues ������������������������������������������������ 153 Mohamed Hassan

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1

Introduction: Dental Implants and Soft Tissues: Roles and Challenges Mohamed Hassan

Dental implants have become a widely accepted modality for replacing missing teeth to fulfill both the functional, aesthetic, and other needs of patients. Adequate supporting structures (bone and soft tissues) are essential to achieving high implant success rates. While adequate quantity and quality of bone play a major role in the short and long-term implant support, proper soft tissue management contributes to both functional and aesthetic outcomes. This book highlights different modalities and techniques for handling soft tissues from the surgical phase and through and beyond the restorative phase. The aim of the book is to provide dentists who are involved in dental implants with an overview of how to deal with challenges they may face regarding soft tissues as related to supporting the placement of implants.

1.1 Multi-Stakeholder and Multifactor Approaches to Supporting the Management of Soft Tissues Tooth loss can pose a challenge to patients and negatively affect many aspects of their lives, including social, physical, and mental health. Due to the importance of the presence of teeth to facilitate chewing food, phonetics, and aesthetics, edentulism may negatively impact the quality of life. Dentists across specialties and other dental professionals (e.g., hygienists, dental assistants) ongoingly need to expand our knowledge base in order to meet patients’ priorities and circumstances in manners that fit their lifestyle and maintain an acceptable quality of life throughout the process. Patients expect their dental care

M. Hassan (*) Oral Medicine, Infection & Immunity, Harvard School of Dental Medicine, Boston, MA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_1

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providers to be able to discuss different treatment options with them and help them make choices that best fit their needs. For dentists to effectively meet patients’ needs, they should be familiar with different methods of tooth replacement and the advantages and limitations of each option as pertaining to the circumstances of each patient. Currently, dental implants are considered the option that most patients and dental health care providers consider the closest match to natural dentitions. If patients opt to have implants replace their missing teeth, it becomes essential to establish a dialogue to discuss how to implement logistical steps to promote success. Patients and members of the dental team need to be familiar with all the treatment steps involved in order to avoid misunderstandings, lack of coordination, and other unsatisfactory outcomes for all parties. Successful outcomes are a shared responsibility between patients and their dental care team. Promoting a high success rate of implants is a multifactorial process. Some factors are related to the patient’s medical, dental, anatomical, and functional conditions. Other factors are related to the ability of the dental team to prepare and deal with clinical findings during different stages of implant placement. One of the most important factors that significantly affects the success rate of dental implants is the presence of adequate and healthy hard and soft tissues. This textbook focuses on the soft tissues around dental implants and varied techniques of dealing with their lack of quantity or quality. Bringing together medical doctors and dentists, we provide a holistic perspective on how all members of the dental team can collaborate across the surgical, restorative, and even maintenance phases to support positive outcomes and increase the success rate of dental implants.

1.2 Overview of Chapters The chapters outline ways to deal with multiple aspects of soft tissue deficiencies to ensure the proper quantity and quality surrounding dental implants. In addition to helping correct existing problems, the chapters address ways to maintain healthy conditions once achieved in order to prevent potential future deformities. Achieving and maintaining healthy soft tissues will help increase the implant success rate with increased longevity. In particular, Chap. 2 (Hassan, A) describes that in order to make a sound and clear treatment plan, practitioners need to familiarize themselves with the histology and anatomy of different types of oral soft tissues. Without adequate and correct anatomical and histological knowledge, clinicians may face challenges in how to diagnose and manage the clinical situation based on a patient’s needs and circumstances. The overview of histology and anatomy provides the foundation for Chap. 3 (Jeong), which focuses on the role of soft tissues in long-term success of dental implants. Long-term implant success depends on the unique characteristics of each type of soft tissue.

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To achieve long-term success, dentists need to manage short-term challenges, as described in Chap. 4 (Hassan, M.), which describes soft tissue management during different stages of surgical placement of implants. Once dentists determine a deficiency in either the quality and quantity of soft tissues, clinicians usually have multiple chances and phases to augment the quantity and/or improve the quality of existing soft tissues surrounding the site of the implant before, during, and after its placement. Chapter 4 reviews multiple methods and techniques that can be utilized in various stages in case an aspect of supporting soft tissues is not completed at a particular stage. Having a range of methods and opportunities to implement them, including the surgical or even after loading the implants, allows practitioners to choose the most applicable or appropriate method based on clinical evaluation and timing of the procedure. Once the implant is placed and/or loaded, Chap. 5 (Kim and colleagues) stresses the importance of maintenance to help continue its success. Routine maintenance visits and proper oral hygiene measures are needed to maintain healthy soft tissue around dental implants and promote the longevity of the implant. Maintenance of dental implants includes periodic clinical and radiographic evaluations to facilitate early detection of and dealing with potential failure or negative signs or symptoms. Periodic visits also allow dental care providers to achieve adequate patient compliance and knowledge of home care and oral hygiene instructions with the use of different brushing techniques and hygiene instruments. These nonsurgical measures minimize the need for more invasive surgical techniques. Despite all the measures taken to ensure healthy and adequate soft tissues, practitioners who are involved in dental implant work may encounter soft tissue pathology, which may affect the longevity and success of the implants. Chapter 6 (Alaskar) offers an overview of the most common pathologic lesions and proper surgical and nonsurgical measures to manage them. In cases of soft tissue pathology, treatment planning should be determined through consultations between clinicians (e.g., general dentists, pathologists, and implantologists). Implants may show signs and present symptoms of failure and or adverse outcomes and different stages during the complete treatment journey. While the surgical team is mainly responsible for the first stage of surgical preparation of implant placement, the restorative team will complement the surgical phase by fabricating and inserting a well-fitted, functioning, and aesthetically accepted restoration. In order to provide patients with a comprehensively determined treatment plan that is implemented in a coordinated manner, sound communication between different practitioners is essential throughout the stages of implant placement and its restoration. Assuming the surgical phase is completed, Chap. 7 (Khamis) reviews the prosthetic role in peri-implant during the treatment planning phase. In particular, the chapter outlines relevant theory or rationale and the corresponding methods of prosthetic contribution to peri-implant soft tissue management. The chapter reviews a range of factors that need to be taken into consideration in relation to patient selection, aesthetic treatment planning and implant positioning, and emergence profile while achieving a properly contoured final restoration.

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Adequate knowledge is necessary to help make an educated decision to select between all the available types of restoration. Chapter 8 (Khamis) presents the steps involved in the selection between various prosthetic designs and their effects on peri-implant soft tissues, whether it is screw or cement-retained restoration. Finally, once the implant has been restored, Chap. 9 (Hassan, M) emphasizes the effects of occlusion on the long-term success and health of dental implants. Inadequate consideration of the effects of occlusion may lead to implant failure in the long term as it may contribute to excessive bone loss and soft tissue inadequacy. After reviewing different types of occlusion, the chapter focuses on traumatic occlusion as a common factor to show its negative effects on implants and their surrounding hard and soft tissues. This volume confirms how implant success requires multifactorial management of soft tissues and other relevant factors by knowledgeable members of the dental team who collaborate effectively with one another and communicate clearly with the patient to set and work towards reasonable expectations about the case. Without adequate knowledge about the role of each member and coordination between them, the results may be compromised, and the outcomes may be unsatisfactory to all dental providers and patients. The high cost to manage and correct undesirable outcomes or to meet the patient’s demands can often be avoided if the patient’s expectations are adjusted to reflect the current situation. Accordingly, this volume highlights different modalities and techniques for handling soft tissues from the surgical phase and through and beyond the restorative phase in order to provide dentists with an overview of how to deal with challenges regarding soft tissues as related to supporting the placement of implants.

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Histology and Anatomy of Different Types of Oral Mucosa Abdelghany Hassan Abdelghany

2.1 Anatomy of the Oral Mucosa The human oral cavity is lined by a mucous membrane (the oral mucosa) that seems to be more complicated than it first appears. The oral mucosa is made up of a stratified squamous epithelium, which may or may not be keratinized. It varies from site to site within the oral cavity, but everywhere the epithelium is protective stratified squamous [1, 2] (Fig. 2.1). The oral cavity has sometimes been described as a mirror that reflects the health of the individual [3]. Changes indicative of disease are seen as alterations in the oral mucosa lining the mouth, which can reveal systemic conditions, such as diabetes or vitamin deficiency, or the local effects of chronic tobacco or alcohol use [4]. Oral mucosa can be divided into three main categories based on function and histology: masticatory, lining, and specialized mucosa. 1. Masticatory mucosa, keratinized stratified squamous epithelium, found on the dorsum of the tongue, hard palate, and attached gingiva [6] (Figs. 2.2, 2.3, 2.4). The hard palate has a partially-keratinized epithelium, much of which is firmly attached by a fibrous submucosa to underlying bone. This epithelium is partially keratinized on gums and hard palate [6] (Figs. 2.1, 2.4).

A. H. Abdelghany (*) Department of Anatomy and Embryology, Faculty of Medicine, Alexandria University, Alexandria, Egypt Faculty of Medicine, Arab Academy for Science, Technology and Maritime Transport, Alamein, Egypt Faculty of Medicine, Alexandria National University, Alexandria, Egypt Anatomy Lead of Manchester Program, Faculty of Medicine, Alexandria University, Alexandria, Egypt e-mail: [email protected] © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_2

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Fig. 2.1  Mouth cavity hard palate soft palate uvula

palatoglossal arch palatine tonsil

Fig. 2.2  Mouth cavity [5]

tongue

palatopharybgeal arch

Lining mucosa gingival crevice

Masticatory mucosa

Tongue mucosa

Fig. 2.3  Lingual mucosa

circumvallate papillae filiform papillae fungiform papillae

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Fig. 2.4 Masticatory mucosa palatine rugae

hard palate

soft palate uvula

a

b

frenulum of tongue sublingual fold sublingual papilla

Fig. 2.5  Buccal mucosa on the cheek (a) and floor of the mouth (b) [8]

2. Lining mucosa, nonkeratinized stratified squamous epithelium, found almost everywhere else in the oral cavity, including the buccal, labial, and alveolar mucosa [6, 7]. (a) Buccal mucosa refers to the inside lining of the cheeks and floor of the mouth [7] (Fig. 2.5). (b) Labial mucosa refers to the inside lining of the lips. It is the moist internal portion of the lip [7] (Fig. 2.6). (c) Alveolar mucosa refers to the covering of the alveolar process of the maxillae and mandible. It is continuous with the mucosa of the cheek, lips, and palate and is loosely attached to the underlying bone [6, 7] (Fig. 2.7). • It is easily distinguished by its bright red color due to many blood vessels and its smooth shiny surface [6]. 3. Specialized mucosa, specifically in the regions of the taste buds on lingual papillae on the dorsal surface of the tongue that contains nerve endings for general sensory reception and taste perception [7] (Figs. 2.3, 2.8).

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Fig. 2.6 Labial mucosa [9]

Fig. 2.7  Alveolar mucosa [9]. (a) Attached gingiva. (b) Alveolar mucosa. (c) Interdental papilla. (d) Free gingiva. (e) Labial frenulum. (f) Mucogingival junction

A. B. C. D. E. F. Fig. 2.8 Specialized mucosa

Attached gingiva. Alveolar mucosa. Interdental papilla. Free gingiva. Labial frenulum. Mucogingival junction. sulcus terminalis

palatine mucosa foramen cecum circumvallate papillae filiform papillae fungiform papillae tip of tongue

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2.2 Histology of the Oral Mucosa The human buccal mucosa is made up of various layers and levels. It contains four independent layers and an underlying connective tissue layer, the lamina propria. The surface is kept moist with mucus produced by the major and numerous minor salivary glands. The oral mucosa is well supplied with nerve endings and, on the dorsal surface of the tongue, special sensory endings for taste [1].

2.2.1 Layers of the Oral Mucosa 2.2.1.1 Stratum Basale The stratum basale (also called the stratum germinativum) is the deepest of the layers of the buccal mucosa. The stratum basale is formed of a continuous layer, usually only one cell thick, of short cuboidal to columnar stem cells. The basement membrane of the cells of this layer is represented by intertwining collagen fibers that help bind these cells to the deeper layers. The cells of the stratum basale, basal keratinocytes, are considered the stem cells of the buccal mucosa. The primary function of these keratinocytes is to divide by going through successive mitotic divisions, generating new cells that migrate superficially to the next superficial mucosal layer, stratum spinosum, in the process of renewal of the mucosal cells. The newly formed cells will undergo a progressive maturation called keratinization as they migrate to the surface of the mucosa [1] (Fig. 2.9). 2.2.1.2 Stratum Spinosum The stratum spinosum (or spinous layer or prickle cell layer) is the layer of buccal mucosa found superficial to the stratum basale and deeper to the stratum granulosum [1, 3]. As the name implies, this layer is spiny in appearance due to the presence of desmosomes, which are protruding cell spiky microfilament projections that join the cells in close contact (Figs. 2.9, 2.10). Fig. 2.9 Schematic illustration of the layers found in the keratinized oral mucosa

stratum corneum stratum granulosum stratum spinosum stratum basale basement membrane

lamina propria

10 Fig. 2.10  Layers of the oral mucosa

A. H. Abdelghany desquamating corneocyte corneodesmosomes lamellar body keratohyalin granules

desmosomes

stratum corneum

stratum granulosum

stratum spinosum

stratum basale

The stratum spinosum is composed of 8 to 10 layers of polyhedral keratinocytes which are formed as a result of successive cell division in the stratum basale. These cells are active in synthesizing fibrillar proteins, known as cytokeratin, which builds up within the cells, aggregating together and forming prominent bundles of keratin microfilaments that go on to form the desmosomes, which allow for strong connections to form between the adjacent keratinocytes. These desmosomes interlock with each other and strengthen the bond between the cells. Therefore, the process of keratinization starts in the stratum spinosum [4, 9]. These spine-like structures are believed to serve as the underlying structural reinforcements that provide strength, elasticity, and flexibility to the layers of the oral mucosa and to better withstand the effects of friction and abrasion. Moreover, the keratinocytes in the stratum spinosum release a water-repelling glycolipid, rendering the mucosa relatively waterproof. As new keratinocytes are produced in the stratum basale, the keratinocytes of the stratum spinosum are pushed upward to the stratum granulosum [4, 9].

2.2.1.3 Stratum Granulosum It is considered a transitional layer sandwiched between the metabolically active layers beneath, stratum basale and stratum spinosum, and the non-viable layer, stratum corneum (containing dead cells) above. It is a thin layer of 3 to 5 cell layers thick. When the keratinocytes are pushed from the stratum spinosum, they become flatter, their cell membranes thicken, and they generate large amounts of the protein keratin, which is fibrous. It is chiefly involved in providing waterproofing function. It also contributes to the keratinization process of the mucosa [4, 9]. It is referred to as the granular layer, as the cells contain irregularly shaped granules. There are two types of granules formed in this layer: the basophilic keratohyalin and the lamellar granules formed by the lamellar bodies (Figs. 2.9, 2.10).

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The basophilic keratohyalin granules contain keratohyalin protein, which is rich in histidine and cysteine. Therefore, the cells are able to generate large amounts of the fibrous protein, keratin. In this way, they seem to be deeply involved in keratinization (formation of keratin) by binding the keratin microfilaments together so that the bundles of keratin become more prominent. Thus, the process of keratinization actually begins in this layer [4, 6]. Also, keratohyalin granules promote dehydration of the cells so that as the cells move toward the stratum granulosum, their nuclei begin to show certain changes, they get flattened with dense masses of nuclear chromatin and early signs of breaking up of the nuclear membrane. It is thought that the lysosomal membranes rupture with the release of lysosomal enzymes, which are responsible for the breakdown of the cells and eventually cause cell death [7, 9, 10]. On the other hand, the lamellar granules secrete a lipid-rich substance that accumulates in the extracellular space between the cells of the stratum granulosum and coats their membranes making them thicker. This lipid-rich material ensures that the cells are firmly connected together and also forms a waterproof barrier. In other words, the lipids by acting as water sealant make the layer waterproof, and moreover, also reduce its permeability and prevent water and water-soluble substances from passing through and entering the lower layers. Penetration of any foreign material or microbes is also not possible [11, 12] (Figs. 2.9, 2.10). At the transition between this layer and the stratum corneum, the nuclei and other cell organelles disintegrate and the cells die, leaving dark cytoplasmic material and densely packed keratin filaments within the cell membranes. So, when these nonviable cells reach the above layer (stratum corneum), they turn dead and fully packed with keratin and now they are called corneocytes [9].

2.3 Stratum Corneum The stratum corneum is the most superficial and exposed layer of the oral mucosa. The increased keratinization (also called cornification) of the cells in this layer gives it its name. There are usually 15–30 layers of cells in the stratum corneum. This dry, dead layer helps prevent the penetration of microbes and the dehydration of underlying tissues and provides mechanical protection against abrasion for the more delicate, underlying layers. Moreover, it is the keratin that makes the mucosa flexible and strong. Cells in this layer are shed periodically and are replaced by cells pushed up from the stratum granulosum [9] (Figs. 2.9, 2.10).

2.3.1 Movement of Keratinocytes from the Stratum Basale to the Superficial Layers As new cells are produced in the stratum basale, the keratinocytes of the stratum spinosum are constantly being pushed toward the next layer, the stratum

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granulosum, where the keratinocytes secrete keratin and lipids that serve as the skin’s waterproof barrier. Then, the cells begin to lose their nuclei and organelles and become dead in the outermost layer, the stratum corneum. It takes approximately 14 days for a cell to migrate from the stratum basale to the stratum corneum and further 2 weeks for the cells to cross the stratum corneum to the surface, where they finally are shed. Injury and inflammation increase the rate of proliferation and maturation [9].

2.4 N.B. Most of the oral mucosa consists of parakeratinized epithelium, which contains nucleated keratinocytes. Parakeratinized epithelium is a term usually used for partially keratinized epithelium that doesn’t have several layers of dead cells at the surface, as may be found in the oral cavity. Parakeratinized epithelium is similar to keratinized epithelium, except that in parakeratinized epithelium, cell nuclei are present in the stratum corneum. An example is the masticatory mucosa located on the hard palate and gingiva [11–13].

2.4.1 The Lamina Propria It is a layer of fibrous connective tissue that consists of a network of collagen fibers (type I and III). Fibroblasts represent the main cells of the lamina propria, and they are responsible for the production of fibers as well as the extracellular matrix. Other cells, such as lymphocytes, plasma cells, and mast cells, are also present [10, 13] (Fig. 2.11). The lamina propria helps provide support and nutrition to the epithelium, as well as a means to bind to the underlying tissue [13]. The lamina propria has two layers: papillary and dense. (a) The papillary layer is the superficial layer. It consists of connective tissue papillae containing loose areolar connective tissue, along with blood vessels and nerves [12, 13]. (b) The dense layer is the deeper layer of the lamina propria. It consists of dense connective tissue with a large amount of fibers [13] (Fig. 2.11). A submucosa may or may not be present deep to the dense layer of the lamina propria, depending on the region of the oral cavity, and it overlies the bones. If present, the submucosa usually contains loose areolar connective tissue with blood vessels and nerves and may also contain adipose tissue or minor salivary glands [10] (Fig. 2.11).

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Epithelium papillary layer

Lamina propria reticular layer

Submucosa

Periosteum Bone

Fig. 2.11  Lamina propria and submucous layer of the oral mucosa [14]

References 1. Nancy A. Structure of the oral tissue. In: Ten cate’s oral histology, development, structure and function. 8th ed. Elsevier; 2013. p. 280. 2. Drake RL, Vogl AW, Mitchell AWM, Tibbitts RM, Richardson PE. Head and neck. In: Gray’s atlas of anatomy. Chirchill Livingstone, International ed; 2008. p. 428–538. 3. Rosengard HC, Messadi DV, Mirowski GW. Oral manifestations of systemic diseases at eMedicine. 2018. 4. Squier CA, Kremer MJ. Biology of oral mucosa and esophagus. J Natl Cancer Inst Monogr. 2001;29:7–15. 5. Proksch E, Brasch J. Tissue specific immunity at the oral mucosal barrier. Trends Immunol. 2018;39(4):276–87. 6. Chandra S, Chandra S, Chandra M, Chandra G, Chandra N. Textbook of dental and oral histology and embryology with MCQs. 2nd ed. New Delhi: Jaypee Brothers; 2010. p. 180. 7. Fehrenbach M, Popowics T. Illustrated dental embryology, histology, and anatomy. 4th ed. St. Louis, MI: Elsevier; 2015. p. 106. 8. Kal BI, Evcin O, Dundar N, Tezel H, Unal I. An unusual case of immediate hypersensitivity reaction associated with an amalgam restoration. Br Dent J. 2008;205(10):547–50. 9. Berkovitz BK, Holland GH, Moxham BJ. Oral anatomy, histology and embryology. 3rd ed. Mosby; 2002. p. 220–48.

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10. Young B, Lowe JS, Stevens A, Heath JW. Wheater’s functional histology: a text and colour atlas. 5th ed. Amsterdam: Elsevier; 2007. p. 251–62. 11. Presland RB, Dale BA. Epithelial structural proteins of the skin and oral cavity: function in health and disease. Rev Oral Biol Med. 2000;11(4):383. 12. Presland RB, Jurevic RJ.  Making sense of the epithelial barrier: what molecular biology and genetics tell us about the functions of oral mucosal and epidermal tissues. J Dent Educ. 2002;66(4):564. 13. Junqueira LCU, Carneiro J. Basic histology text & atlas. Lang Des. 10th ed; 2003. p. 187. 14. Sapna K, Renuka D, Gholve S. Challenges face by pharmaceutical industry for the development of oral film dosages form. Int J Pharm Pharm Res. 2017;10(1):1.

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The Role and Importance of Soft Tissues for Long-Term Success of Dental Implants Y. Natalie Jeong

The demand for dental implants continues to grow because more providers and patients are viewing dental implants as a predictable therapeutic treatment option. With more patients receiving dental implant treatments, treating clinicians are observing more complications and adverse events as well [1–3]. Therefore, the long-term efficacy of dental implants must be carefully assessed. Criteria such as marginal bone level, patient comfort level, and sulcus depth have been used to define the long-term success of implant therapy [1, 2]. Although osseointegration has traditionally been considered the most important factor in maintaining implant stability, the roles of transmucosal healing and health around the implant are also being considered as determining factors that influence long-term implant success [3, 4]. Peri-implant mucosa that forms during the wound healing process following implant placement is the corresponding term for biological width around natural teeth [5, 6]. The basic function of the peri-implant mucosa is to protect the underlying bone that supports the implant [7]. The average peri-­ implant mucosal dimension is 3 mm, which is 1 mm longer than the biologic width of natural teeth [8]. Although it has been controversial for many years, the preponderance of evidence suggests that a minimum dimension of peri-implant mucosa is crucial in maintaining long-term implant health. Invasion of the peri-implant mucosa results in tissue inflammation and potential bone loss [8–11], and the breakdown and loss of peri-implant tissue can compromise the long-term success and survival of the implant [7]. The soft tissue attachment apparatus around dental implants is significantly different from that of natural teeth [12, 13]. In natural teeth, the root of the tooth is covered by a root cementum from which collagen fibers run perpendicular to the long axis of

Y. N. Jeong (*) Department of Periodontology, Tufts University School of Dental Medicine, Boston, MA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_3

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the tooth and attach to the surrounding hard and soft tissues. An implant has no cementum, and the collagen fibers are oriented parallel to the long axis of the implant without direct anchorage [12–14]. Therefore, the peri-implant soft tissues are more fragile during the inflammatory process [15, 16]. Clinical soft-tissue parameters such as tissue phenotype, amount of keratinized mucosa, and tissue thickness have been considered important factors that influence long-term implant success [17–20]. According to a study that examined peri-implant mucosal dimension using bone sounding around the implants, a peri-implant mucosal dimension at the facial aspect of less than 3 mm was associated with a thin biotype. A thick biotype was observed when there was a periimplant mucosal dimension of more than 4 mm at the facial aspect. Implant restoration may be prone to papilla loss when the distance from the tip of the papilla to the bone of the adjacent tooth is greater than 4 mm in a thin biotype [5]. To maintain long-term stable implant health, a minimum peri-implant dimension is necessary. Violation of peri-implant mucosa causes peri-implant tissue inflammation and marginal bone loss, and angular defects may develop [9–12].

3.1 Peri-Implant Phenotype The peri-implant phenotype is defined as “the morphologic and dimensional features characterizing the clinical presentation of the tissue that surround and support osseointegrated implants” [21]. The components of the peri-implant phenotype are keratinized mucosa width (KMW), mucosal tissue thickness (MTT), and supracrestal tissue height (STH). The peri-implant bone thickness makes up the osseous component of the peri-implant phenotype [21] (Fig. 3.1). This description applies to

Mucosal Margin A1

Keratinized Mucosa Width (KMW)

A2

Mucosal Thickness (MT)

A3

Supracrestal Tissue Height (STH)

B1

Peri-Implant Bone Thickness (PBT)

A2 A3

B1

A1

Peri-Implant Bone Crest Mucogingival Junction

Fig. 3.1  The components of the peri-implant phenotype (adapted from Avila-Ortiz G, Gonzales-­ Martin O, Couso-Queiruga E, Wang HL [21])

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the lingual and facial aspects of the implants. The peri-implant phenotype is site-­ specific and may change because of external factors [21]. The thick labial peri-­ implant phenotype is present when there is a thick buccal plate [17]. Furthermore, the peri-implant soft tissue phenotype may be modified with surgical interventions [22]. Therefore, clinicians may consider intervention by means of bone augmentation before or during implant placement when a thin buccal plate is present [17].

3.2 Keratinized Mucosa Width Keratinized mucosa extends from the margin of the peri-implant mucosa to the oral mucosa [23]. The peri-implant KMW is the most coronal part of the peri-implant soft tissues [21]. The need for adequate width of keratinized mucosa around dental implants has been studied by many researchers and remains somewhat controversial [20, 24–31]. At present, the consensus seems to be that an adequate KMW is associated with low plaque accumulation and improved soft tissue health (Fig. 3.2). Several studies have shown that in subjects with KMW a greater than 2 mm, the Modified Plaque Index and Modified Gingival Index were higher and the Plaque Index and Gingival Index were lower [20, 27, 31–36]. When probed, implants with a narrow zone of keratinized mucosa tend to bleed more than implants with a wider zone of keratinized mucosa [30, 37, 38]. It has been revealed that implants with a KMW less than 2 mm showed more plaque accumulation and that they were more likely to sustain tissue breakdown, leading to earlier loss of attachment [15, 16, 30, 37, 39]. Pain during home care was reported more frequently by the patients with inadequate KMW at implant sites. This could be caused by mechanical irritation resulting from the mobility of non-keratinized tissue when stimulated by a toothbrush [30]. However, it has also been observed that peri-implant health can be sustained in the presence of inadequate KMW (less than 2 mm) in patients who practice meticulous oral hygiene [28, 29]. Dental implants without adequate KMW, combined with high levels of plaque accumulation, had a greater incidence of peri-­ implantitis [28, 37–39]. Furthermore, it was found that gingival recession was greater around implants that were not surrounded by adequate KMW compared to the implants with adequate KMW (Fig. 3.3) [31, 32, 36, 38]. Keratinized mucosa Fig. 3.2  #4 implant with adequate KMW with healthy peri-implant tissue (Photo courtesy of Dr. Andreas Parashis)

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Fig. 3.3  Implant with inadequate KMW and recession (Photo courtesy of Dr. Andreas Parashis)

width can be a key parameter to measure in the timely identification of mucosal recession of dental implants [32, 40]. However, it has been suggested that inadequate KMW may be a consequence of recession, rather than the precipitating factor for worsening of a site [32, 38, 41]. In conclusion, although an adequate KMW may not be a prerequisite for long-term implant health, the presence of adequate KMW may reduce the occurrence of peri-implant tissue inflammation and the breakdown of peri-implant mucosa.

3.3 Mucosal Tissue Thickness Peri-implant mucosal tissue thickness (MTT), the horizontal dimension of soft tissue, can be measured with a probe at approximately 1.5 mm apical to the soft tissue margin at the base of the probing depth. MTT extends from the external soft tissues to the internal hard surfaces. Peri-implant MTT may or may not be keratinized and does not necessarily correspond to the height of the keratinized tissue. The soft tissue thickness is closely related to the peri-implant phenotype. The dimension may vary from location to location (e.g., facial versus lingual) [21, 42]. The midfacial aspect of the tissue thickness is affected by the implant’s shoulder location [43]. The thickness of the peri-implant tissue plays a significant role in the long-term success of implant therapy, as well as functional and esthetic outcomes [21, 44–46]. Implants with thin crestal mucosa tend to have more marginal bone loss than implants with adequate crestal mucosa [47, 48]. Mucosal tissue thickness plays a more significant role in minimizing marginal bone loss with implants that were placed supracrestally compared to implants that were placed at the level of the crest [49, 50]. This could be because of the different locations of the interface between the implant fixture and the implant abutment. Implants with crestal placement have a microgap that is very close to the bone, and marginal bone loss may occur because of potential bacterial microleakage [49]. Implants with mucosal tissue thickness of more than 2 mm, as measured horizontally and perpendicularly from the crest, have low marginal bone loss; therefore, it is suggested to perform autogenous or allogenic tissue grafting to minimize early

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marginal bone loss [48, 51, 52]. Soft tissue grafting procedures to increase mucosal tissue thickness minimize interproximal marginal bone loss overtime [53]. Additionally, successful outcomes have been achieved when soft tissue augmentation was attempted to enhance esthetics and compensate for an underlying osseous defect. The procedure can be performed before or after the loading of the implants [54, 55]. With the effect of the abutment shade on the peri-implant mucosa, the negative visual consequence was minimized in sites with a minimal mucosal tissue thickness of approximately 2 mm [45, 46]. In conclusion, mucosal tissue thickness must be carefully evaluated by clinicians prior to implant placement because implants placed on the sites with thicker peri-­ implant soft tissue tend to sustain less marginal bone loss. Furthermore, thin mucosal tissue is a risk factor for esthetic complications because it compromises the appearance of the shade of the abutment [56]. When the thin tissue is noted, the use of soft tissue augmentation with allograft or autogenous graft should be considered to minimize peri-implant marginal bone loss and improve the esthetic outcome. Clinicians should make every effort to achieve and maintain a minimum of 2 mm of mucosal tissue thickness in daily clinical practice.

3.4 Supracrestal Tissue Height The supracrestal tissue height (STH) is the “vertical dimension of the soft tissue,” which runs from the mucosal margin to the bone crest; this is assessed “circumferentially” around an implant, at both proximal sites and buccal and lingual aspects [21]. This characteristic can be measured by transmucosal sounding with a periodontal probe [56]. “Vertical soft tissue thickness on crestal bone” is another term that is used to refer STH [51]. The sulcular epithelium, the junctional epithelium, and the supracrestal connective tissue are engirdled in the peri-implant STH. The supracrestal connective tissue is not directly attached to the implant abutment surface [21]. The dimension of the peri-implant STH is different from its counterpart, the supracrestal tissue attachment of the tooth, in that it is taller by 1 to 1.5 mm in all buccal/lingual and proximal aspects. It is typically greater in interproximal areas [23]. An inadequate STH at the time of implant placement surgery is a predisposing factor for early marginal bone loss [47, 48, 51], regardless of the type of implant (e.g., bone level implant, tissue level implant, or implant with platform switching) [21]. This is probably due to the physiologic organization of implant-supporting elements during the initial healing period [21]. It has been suggested that a practical cut-off value to distinguish between favorable and unfavorable STH should be 2–3 mm in clinical practice [21, 50, 57, 58]. An adequate STH is associated with greater papillary volume and is determined by the connective tissue adhesion level at the adjacent interproximal tooth surface [5, 59, 60]. It is about 3 mm between two adjacent implant restorations, and it is extremely unpredictable and challenging to regenerate [56]. Therefore, an interproximal space morphology should be carefully assessed prior to the implant placement to plan an ideal esthetic outcome [56, 61].

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In conclusion, the STH reestablishes an anatomical space for the implant-­ supporting apparatus, and adequate STH dimension is crucial for long-term peri-­ implant health. Both functional and esthetic outcomes can be improved by careful examination and possible modification of the STH architecture.

3.5 Peri-Implant Soft Tissue Phenotype Modification and Its Influence on the Long-Term Success of the Implant Peri-implant phenotype influences the esthetic and functional long-term outcomes of implant treatment [21, 23, 27, 28, 46, 51, 53, 57]. A thin peri-implant mucosa, as measured by the supracrestal tissue height, is correlated with greater marginal bone loss than a thick tissue phenotype [47, 48, 51]. In clinical practice, horizontal and vertical ridge resorption following tooth extraction is commonly observed [62, 63]. Clinicians often perform bone augmentation procedures along with implant surgery; this may induce a coronal displacement of the mucogingival junction, which has a negative effect on peri-implant soft tissue dimension [63, 64]. The following protocols have been suggested as intervention points for soft tissue augmentation: prior to implant placement, at the time of implant surgery, after implant placement but prior to second stage surgery (Fig. 3.4),

Fig. 3.4  Free gingival graft to increase keratinized gingiva prior to second-stage surgery (Photo courtesy of Dr. Theresa Sun)

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Fig. 3.5  Free gingival graft at the time of second-stage surgery (Photo courtesy of Dr. Giac Dang)

at the time of stage two (implant uncovering) surgery (Fig. 3.5), and after the implant is already uncovered. Intervention after an implant is restored is not recommended unless intervention is required due to peri-implant tissue inflammation [63]. Several techniques to increase the peri-implant soft tissue phenotype, including KMW, MTT, and STH, have been suggested [21, 46, 53]. Autogenous free gingival graft and autogenous connective tissue graft have historically been the first therapy of choice because of their proven efficacy around natural dentition [22, 65]. Free gingival grafts not only increase KMW but also deepen the vestibule during the recipient bed preparation. Due to this additional benefit, the free soft tissue graft technique is the preferred therapy when planning an implant-assisted prosthesis, such as implant-supported overdentures [66]. When using a free gingival tissue graft, an apically positioned flap technique should be employed rather than a bilaminar technique because it has been reported that KMW did not significantly increase following the bilaminar technique with free gingival graft [22, 67]. In a study on dogs, free soft tissue autograft (i.e., free gingival graft) placed at an implant site resulted in a greater KMW gain than an apically positioning flap or xenogenic collagen matrix [66, 68]. Connective tissue grating increases mucosal tissue thickness in addition to supracrestal tissue height [22, 66]. This grafting procedure is particularly helpful because it improves the esthetic outcome as well as peri-implant tissue health [22, 65, 67].

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To minimize patient morbidity and eliminate a second surgical site for the donor tissue, different allograft and xenograft techniques are also utilized [22, 67, 69]. An acellular dermal matrix can be used to increase keratinized mucosa width and mucosal tissue thickness [22, 67, 70–72]. Although a connective tissue graft is considered the gold standard for the grafting material of choice when augmenting peri-­ implant soft tissue, an acellular dermal matrix is reported to accomplish comparable mucosal tissue thickness gain as well as increase supracrestal tissue height [22, 47, 67, 70, 73]. A xenogenic collagen matrix has also been used as an alternative for autogenous connective tissue grafting. This material has been known to increase keratinized mucosal width and mucosal tissue thickness [22, 70–72]. When a bilaminar approach is utilized, peri-implant soft tissue phenotype modification with a xenogenic collagen matrix can stabilize marginal bone levels [22, 74]. Therefore, both allogenic and xenogenic soft tissue grafts are considered adequate and safe alternatives, and they may improve treatment acceptance by reducing patient concerns for donor site discomfort and the need for a second surgical site [66].

3.6 Concluding Remarks The role of peri-implant soft tissue on the long-term health of the implant has historically been considered somewhat controversial. However, most evidence suggests that a thick peri-implant phenotype, wide band of keratinized mucosa, adequate mucosal tissue thickness, and adequate supracrestal tissue height may reduce peri-implant tissue inflammation and future functional and esthetic complications [17, 56, 66]. Clinicians should carefully examine peri-implant phenotypes when planning implant therapy and, if necessary, should create a favorable peri-­ implant architecture by employing peri-implant soft tissue phenotype modification.

References 1. Smith DE, Zarb GA. Criteria for success of osseointegrated endosseous implants. J Prosthet Dent. 1989;62:567–72. 2. Proskin HM, Jeffcoat RL, Caitlin A, et al. A meta -analytic approach to determine the state of the science on implant stability. Int J Oral Maxillofac Implants. 2007;22(suppl):11–8. 3. Jung RE, Sailer I, Hammerle CH, et al. In vitro color changes of soft tissues caused by restorative materials. Int J Periodontics Restorative Dent. 2007;27:251–7. 4. Lindhe J, Lang NP, Karring T. The mucosa at teeth and implants. Clin Periodontol Implant Dent. 2008;Chapter 3:71–7. 5. Kan JY, Rungcharassaeng K, Umezu K, et al. Dimensions of peri-implant mucosa: an evaluation of maxillary anterior single implants in humans. J Periodontol. 2003;74:557–62. 6. Lee A, Fu JH, Wang HL.  Soft tissue biotype affects implant success. Implant Dent. 2011;20(3):e38–47. 7. Derks J, Hakansson WJL, et al. Effectiveness of implant therapy analyzed in a Swedish population: early and late implant loss. J Dent Res. 2015;94:44S–51S.

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8. Cochran DL, Hermann JS, Schenk RK, et al. Biologic width around titanium implants. A histometric analysis of the implant-gingival junction around unloaded and loaded nonsubmerged implants in the canine mandible. J Periodontol. 1997;68:186–98. 9. Sanavi F, Weisgold AS, Rose LF.  Biologic width and its relation to periodontal biotypes. J Esthet Dent. 1998;10:157–63. 10. Berglundh T, Lindhe J. Dimension of the peri-implant mucosa. Biological width revisited. J Clin Periodontol. 1996;23:971–3. 11. Berglundh T, Abrahamsson I, Welander M, et al. Morphogenesis of the peri-implant mucosa: an experimental study in dogs. Clin Oral Implants Res. 2007;18:1–8. 12. Abrahamsson I, Berglundh T, Wennstrom J, Lindhe J. The pero-implant hard and soft tissues at different implant systems. A comparative study in dog. Clin Oral Implants Res. 1996;7:212–9. 13. Lindhe J, Berglundhe T.  The interface between the mucosa and the implant. Periodontol. 2000;1998(17):47–54. 14. Charpure AS, Latimer JM, Alijofi FE, et al. Role of thin gingival phenotype and inadequate keratoinized mucosa width ( 10.1) was shown to be associated with increased bleeding on probing at implants [15]. Ferreira et al. [16] also reported an association with peri-implant mucositis and systemic disease. However, the systemic diseases described included “diabetes mellitus, hormonal changes, menopause, chemotherapy, thyroid alterations, cardiac problems, and alcohol use,” and thus the results of the study are difficult to interpret.

6.5.3 Diagnosis Criteria The main clinical characteristics of peri-implant mucositis include bleeding on gentle probing; erythema, swelling, and/or suppuration may also be present. An increase

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in probing depth is often observed in the presence of peri-implant mucositis because of swelling or a decrease in probing resistance, which needs to be considered to avoid misdiagnosis. The absence of bone loss beyond crestal-bone-level changes, confirmed by radiographs, indicates alterations resulting from initial bone remodeling. There is strong evidence from animal and human experimental studies that plaque is the etiological factor for peri-implant mucositis and can be resolved by nonsurgical periodontal therapy [17]. The diagnosis of peri-implantitis requires the presence of bleeding and/or suppuration on gentle probing, an increase in probing depth compared to previous examinations, and the presence of bone loss beyond the crestal bone levels. In the absence of previous examination data, diagnosis of peri-implantitis can be based on the combination of the following: the presence of bleeding and/or suppuration on gentle probing, probing depths of ≥6 mm, and bone levels ≥3 mm apical to the most coronal portion of the intra-osseous part of the implant [18].

6.5.4 Treatment of Peri-Implant Mucositis and Peri-Implantitis Peri-implant mucositis is primarily caused by a disruption of the host–microbe homeostasis at the implant–mucosa interface and is a reversible condition at the host biomarker level. Regular supportive peri-implant therapy with biofilm removal is an important first preventive strategy against the conversion of health to peri-­ implant mucositis and also against the progression of peri-implant mucositis to peri-­ implantitis [17]. In addition to the biofilm removal, it is very substantial to determine the goal of therapy for both peri-implant mucositis and peri-implantitis, which is usually confined to control of the bacterial etiology, elimination of soft tissue inflammation, implant surface decontamination, regenerative approach, resective approach, implant surface modification (implantoplasty), and re-osseointegration [19]. Furthermore, it is important to take into consideration the limitations of the therapy, ranging from accessibility, implant configuration, implant surface structure, soft tissue conditions, defect configuration, and grafting materials to the amount of bone loss [20, 21]. As mentioned earlier, biofilm removal by nonsurgical mechanical debridement (MD) is the first treatment procedure for the treatment of peri-implant mucositis along with local chemotherapeutic antiseptic agents. There are numerous therapies, such as antibiotic and probiotic therapy, laminin coatings on implant surfaces, low-­ level laser therapy, and photodynamic therapy (PDT), that have been assessed as adjuncts to MD for the treatment of peri-implant diseases [22–27]. Photodynamic therapy (PDT) is another form of local therapy that has been used as an adjunct to MD for peri-implant diseases in several studies [23, 28–31]. In this form of adjunct therapy, a dye (photosensitizer) is locally delivered to the peri-­ implant sulci of infected sites and is then exposed to a laser with a wavelength usually ranging between 660 to 800 nm [32]. The resultant reaction produces reactive oxygen species (ROS), which possibly reduce inflammation and counts of

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pathogenic microbes at the treatment sites, thereby facilitating the overall healing process. Studies [29, 33] have explored the contribution of PDT as an aide treatment to routine oral hygiene maintenance instructions for the treatment of periodontal and peri-implant diseases. It has also been proposed that MD with adjunct PDT is more effective in reducing peri-implant soft tissue inflammation (peri-implant mucositis) than MD alone [34]. In cases of peri-implant mucositis, the etiology attributed to the lack of keratinized tissue (KT) surgical periodontal treatment, including gingival graft after the phase of MD, is considered. Although there was debate in the dental literature about the prevalence of peri-implant soft tissue diseases and lack of KT, an increase in the width of KT may be considered in order to improve and simplify the patient’s oral hygiene and to preserve the level of mucosal tissue [35–37]. For dental implants and natural teeth alike, the value of having an acceptable width and density of KT tends to be important, comparably to teeth without KT, which were observed to be more vulnerable to more impairment of attachment [38]. Tissue breakdown has also been found to develop more rapidly with dental implants than with teeth [39] (Figs. 6.4 and 6.5). Peri-implant mucositis, the most common soft tissue pathology around dental implants, seems to be a precursor to subsequent peri-implantitis. The treatment during the transitional stage typically involves antibacterial therapy, combined with

B-Wide zone/band of keratinized tissue KT

A-Inadequate zone/band of keratinized tissue KT

Fig. 6.4  Schematic drawing presenting the differences between A inadequate zone of keratinized tissue (KT) and B wide zone of KT

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Fig. 6.5 (a) Labial view of a two-implant-supported overdenture with a lack of keratinized attached gingiva and peri-implant mucositis. (b) Free gingival graft done around a two-implant-­ supported overdenture to increase the zone of keratinized attached gingiva and enhance patient oral hygiene practice

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Fig. 6.6  Cumulative Interceptive Supportive Therapy (CIST) by Lang 1997. Depending on peri-­ implant probing depth (PDD), plaque index, bleeding on probing (BOP), and cratering with guided four treatment options according to the clinical and radiographic findings. Treatment A is mechanical cleansing using rubber cups, polishing paste, and acrylic sealers for chipping-off calculus. Instruction for more effective oral hygiene practices, Treatment B is antiseptic therapy. Rinses with 0.1–0.2% chlorhexidine digluconate for 30 s using approximately 10 mL, for 3–4 weeks supplemented by irrigating locally with chlorhexidine (preferably 0.2–0.5%) using a Luer syringe or local chlorhexidine gel application. Treatment C is antibiotic therapy 1-systemic ornidazol (2 × 500 mg/die) or metronidazole (2 × 250 mg/die) for 10 days or a combination of metronidazole (500  mg/die) plus amoxicillin (375  mg/die) for 10  days. 2. Local: Application of slow-release devices for 10 days (25% tetracycline fibers). D Surgical approach 1. Regenerative surgery using abundant saline rinses at the defect, barrier membranes, close flap adaptation, and careful postsurgical monitoring for several months. Plaque control is to be assured by applying chlorhexidine gels. 2. Resective surgery. Apically repositioning of the flap following osteoplasty around the defect

MD before attempting surgical regeneration of peri-implant alveolar bone lost due to infection. Lang et al. in 1997 [40] published a review of clinical trials on therapies for peri-implant infections, revealing that the inflammatory process in soft and mineralized peri-implant tissues can be controlled. This renders the site susceptible to regenerative procedures aimed at re-establishing osseointegration after nonsurgical therapy and the administration of local and systematic antibiotics. However, as of today, no controlled studies have been performed to document the possibility of true osseointegration [20, 41, 42]. A previous cited study [40] proposed a well-­ documented system for the management of peri-implant diseases called cumulative interceptive supportive therapy (CIST). This approach is very helpful for the development of a joint effort for the management of soft and hard tissue conditions (Fig. 6.6). Surgical treatment therapy for peri-implantitis, as it is the progressive disease of the common soft tissue pathology around dental implants, is mainly a regenerative approach [43]. The treatment consisted of flap reflection, surface decontamination, use of enamel matrix derivative (EMD) or platelet-derived growth factor (PDGF),

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and guided bone regeneration with mineralized freeze-dried bone and/or anorganic bovine bone combined with PDGF or EMD and covered with an absorbable membrane and/or subepithelial connective tissue graft (Fig. 6.7). However, the destructive soft tissue pathological inflammatory process affects both soft and hard tissues, leading to pocket formation and progressive bone

a

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Fig. 6.7  Soft tissue fistula around the implant of upper right first premolar with bone loss. (a) Pre-surgical view showing the soft tissue fistula. (b) surgical view showing the soft tissue granulation around the dental implant. (c) Surgical view showing the bone loss and defect around the dental implant after degranulation. (d) Peri-implant bone graft with a membrane around contained bony defects of the implant. (e) Membrane adaption above the bone graft and implant. (f) Primary coverage with EPTF suture. (g) Second stage and connection of the healing abutment after 4 months post-surgical. (h) Pre-surgical radiograph showed mesial and distal vertical bone loss around the dental implant. (i) Post-surgical radiograph after bone graft. (j) 4 months post-surgical bone graft showed bony filled

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h

i

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Fig. 6.7 (continued)

resorption around osseointegrated oral implants. Explanation may be indicated in advanced stages with severe bone loss when soft tissue pathology cannot be eradicated with re-augmentation of the site for new implant placement and restoration (Fig. 6.8) [44]. According to published studies [16, 45], peri-implant diseases are very common. Therefore, it is imperative for the clinician to examine and evaluate patients who have been provided with implant-supported restorations on a regular basis. The following aspects are recommended for the clinical routine: When implant treatment is considered, patients should be informed of the risks for biological complications (peri-implant diseases) and the need for preventive care. An individual risk assessment, including systemic and local risk indicators, should be performed, and modifiable risk factors, such as residual increased probing pocket depth in the remaining dentition or smoking, should be eliminated. Hence, treatment of periodontal disease aiming for elimination of residual pockets with bleeding on probing and smoking cessation should precede implant placement [46].

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a

b

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Fig. 6.8  Destructive soft tissue pathological inflammatory process affects both soft and hard tissues, leading to implant failure of the area of the upper left first premolar. (a) Pre-surgical view showing the soft tissue inflammation and rolled margin. (b) Pre-surgical radiograph showing an extensive amount of more than 50%. (c) Surgical view showing the pathological soft granulation tissue around the dental implant. (d) Surgical view after implant explanation. (e) Surgical view after complete soft tissue degranulation. (f) Surgical view with two tenting screws to vertically augment the alveolar bone. (g) Radiograph showing labial and palatal vertical tenting screw. (h) Surgical view after bone graft. (i) Surgical view after membrane adaption. (j) Occlusal view after suture and achieving primary coverage. (k) Labial view after suture and achieving primary coverage

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Fig. 6.8 (continued)

The correct fit of implant components and the superstructures has to be ensured to avoid additional niches for biofilm adherence [47]. If cemented implant restorations have been selected, the restoration margins should be located at the mucosal margin in order to allow meticulous removal of excess cement [48, 49]. To facilitate personal oral hygiene, clinicians should consider having keratinized attached surrounding the transmucosal implant portion already during implant

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placement (for one-stage implant placement) or during abutment connection (for two-stage implant placement) [50]. Professional supportive care should be established according to the individual needs of the patient (e.g., 3, 6, or 12-month recall intervals), and their compliance has to be confirmed [51, 52]. Particularly in patients with a history of aggressive periodontitis indicating an increased susceptibility for periodontal and peri-implant diseases, shorter recall intervals should be considered. During recall, peri-implant tissues must be regularly examined, including probing assessments with special emphasis on bleeding on probing [12].

6.6 Reactive Condition That Causes Soft Tissue Pathology Around Dental Implants and Bone Loss 6.6.1 Pyogenic Granuloma Pyogenic granuloma is a common, reactive inflammatory hyperplasia of the oral cavity. Although the term “pyogenic” is used, PG is not an infectious lesion. PG usually occurs as a response to different stimulating factors such as local trauma or irritation and iatrogenic and hormonal factors [10, 53]. Because of the female hormone factor, it has a very high incidence in young females, principally in the second decade of life. Clinically, PG presents as a painless, smooth, or lobulated shape. It is classed as a hemorrhagic lesion because of its vascular structure, and its color ranges from pink to dark red. It is presented clinically as sessile with an average size of 1 cm and has a smooth, shiny surface. In addition, it bleeds very easily when touched. Sometimes, its surface may be covered by a pseudo-membrane due to secondary ulcerations [54]. It was reported that oral PG was found in 18% of patients who had benign oral masses. It was also noted that PG can be observed in individuals as young as 10 years old up to the age of 70 [55]. It is the second most common soft tissue pathology around dental implants after peri-implant mucositis, soft tissue fistula, and peri-­ implantitis. As mentioned previously, local trauma is the main etiological factor, with 30–50% of patients with PG having a history of local trauma. The occurrence of implant-related PG was associated with inappropriate healing caps of implants [56] (Fig. 6.9). Biopsy as a diagnostic approach is warranted because peripheral odontogenic lesions, benign and malignant neoplasms, metastatic lesions, and a variety of other lesions may clinically resemble this reactive nodular lesion of the gingiva. The histopathologic analysis of PG usually reveals an intense vascular proliferation with extensive areas of ulceration, mixed inflammatory infiltrate, numerous granulation tissue, and abundant macrophages (multinucleated giant cells) [57] (Fig. 6.9c). There are several treatment options for PG, such as surgical excision, cryotherapy, electro-cauterization, laser applications, and steroid injections [56]. However,

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a

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Fig. 6.9  Pyogenic granuloma around a dental implant [with permissions from Dr. Emrah Soylu]. (a) Clinical view of PG around a dental implant, 1 month after implant placement. (b) Peri-apical radiograph of the affected site. (c) In the upper left side of the section, the surface epithelium shows regenerative changes. Other sides of the epithelium are ulcerative. Leak connective tissue with edema, proliferative capillary vessels, and aggregation of active-chronic inflammatory cells can be seen at the bottom line of ulceration and in the subepithelial side (hematoxylin and eosin; original magnification 100×). (d) 3 months after the PG surgical removal

providing adequate keratinized soft tissue should be the first step to prevent such lesions for reactive lesions related to dental implants. In addition, management should involve the detection and elimination of the possible local irritant factors, such as abnormal superstructure and healing cap implant relationships or unfavorable implant–bone relationships. Soft tissue site preparation with gingival graft augmentation before implant placement is necessary to enhance the thickness and width of the keratinized gingiva when there is inadequate gingiva thickness and a lack of keratinization (Fig. 6.10) [57].

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a

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Fig. 6.10  Free gingiva graft with apical position flap and vestibuloplasty to increase zone of attached gingiva before ridge augmentation of lower left missing first and second molars. (a) Pre-­ surgical occlusal view showing a lack of keratinized attached gingiva. (b) Pre-surgical lateral view. (c) Surgical view showing the recipient site preparation. (d) Surgical view showing donor tissue FGG suturing and adapted in the recipient site. (e) 2 weeks post-surgically before suture removal. (f) Post-surgical occlusal view showing the amount of keratinized attached gingiva gain. (g) Post-­ surgical lateral view indicating the zone of attached gingiva in preparation for guided bone regeneration followed by future implant placement

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f

g

Fig. 6.10 (continued)

6.7 Autoimmune Conditions That Cause Soft Tissue Pathology Around Dental Implants and Bone Loss 6.7.1 Oral Lichen Planus Oral lichen planus (OLP) is a chronic mucocutaneous inflammatory disease. It affects the skin, nails, hair, and mucous membranes (oral and genital) [58]. It most commonly affects middle-aged individuals, predominantly females [59]. Its prevalence is between 0.1% and 2.2% [60]. OLP is a T cell-mediated autoimmune disorder of uncertain etiology [58, 61]. Besides immune dysregulation, many etiological factors may also be involved, including traumatic insults, medication, dental materials, and stress [62]. It commonly affects buccal mucosa, tongue, and gingiva [63]. Due to the adverse effects of implant placement on LP and vice versa, implant placement should be done with caution [64]. LP patients treated with dental implants are at a risk of implant failure due to the inability of the epithelium to attach to the implant surface, which allows the bacteria to access the preimplant tissue, leading to the failure of osseointegration [65]. It has also been recommended that lichen planus patients be handled with care during the remission phase when the cases are

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stabilized [66]. It should not be placed during the active phase of the LP, which will cause implant failure (Fig. 6.11). Corticosteroids are the main treatment for symptomatically OLP [67]. Topical steroids are considered first-line treatment because they are more effective in treating superficial inflammation, especially in EOLP [59]. Other treatment modalities are being tried to increase the efficacy and decrease the complications of corticosteroids. The therapeutic potential of photodynamic therapy [68] and lasers [69] has been investigated. Ozone therapy is also being used to treat OLP due to its strong antimicrobial activity [67]. Oral corticosteroid dose of 4 mg/daily after insertion of dental implants in patients with suppressed OLP to ensure suppression of the activated immune system is required as an element of the supportive implant therapy (SIT) [70] [Fig. 6.12].

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Fig. 6.11  Active phase of oral lichens planus with implant failure. (a) Clinical view of white striation and ulceration of a patient suffering from active lichen planus. (b) Failed implants placed into a patient suffering from active lichen planus. (With permission from Dr. Moustafa Aboushelib)

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Fig. 6.12  Active phase of oral lichens planus with implant failure. (a) Surgical view of insertion of submerged implants after application of systemic corticosteroids and soft tissue laser irradiation. Notice the complete disappearance of soft tissue symptoms. (b) Implant-supported restoration after 3 years in function. Notice the recurrence of some white striation. (With permission from Dr. Moustafa Aboushelib)

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6.8 Conclusion An adequate treatment plan and supportive periodontal and implant therapy, along with proper oral hygiene care, are the keys to the success of dental implant treatment. However, just like its natural predecessor, a dental implant may be subject to destructive soft and hard tissue pathology. Soft tissue pathology is the first sign of peri-implant diseases. Therefore, in the case of peri-implant soft tissue pathology, the knowledge of the accurate etiology as inflammatory, reactive, or autoimmune is essential to formulating the treatment goals of each clinical case situation. Following the decision trees at the end of this chapter will facilitate the platform form in the field of dental implant practice (Fig. 6.13).

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Decision tree of peri-implant soft tissue management Soft Tissue pathology around dental implant

Inflammatory (peri-implant mucositis and periimplantitis

Following the system for the management of periimplant diseases Cumulative Interceptive Supportive Therapy (CIST)

Reactive

Autoimmune

Pyogenic granuloma

Oral Lichens Planus (OLP)

Identifying and eliminate the etiological causes local trauma latrogenic Hormonal factors

Establish a detailed previous dental history of the OLP

By Lang et al 1997

A- Active Diagnostic approach biopsy is mandating

Topical oral corticosteroi ds and referral to oral medicine

B- Remission Processed with dental implant with maintenance dose of 4 mg oral steroid

Treatment options Surgical excision Cryotherapy Electro- cauterization Laser applications Steroid injections

Accurate follow up

Achieved remission stage Processed as B

Considering then corrective connective tissue graft

Supportive Periodontal and implant maintenance

Fig. 6.13  Decision tree showing the treatment objective and option of the soft tissue pathology around the dental implant

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References 1. Abraham CM.  A brief historical perspective on dental implants, their surface coatings and treatments. Open Dent J. 2014;8:50–5. 2. Schulte W, Kleineikenscheidt H, Lindner K, Schareyka R. The Tubingen immediate implant in clinical studies. Dtsch Zahnarztl Z. 1978;33(5):348–59. 3. Berglundh T, Lindhe J, Ericsson I, Marinello CP, Liljenberg B, Thomsen P. The soft tissue barrier at implants and teeth. Clin Oral Implants Res. 1991;2(2):81–90. 4. Albrektsson T, Eriksson AR, Friberg B, Lekholm U, Lindahl L, Nevins M, et al. Histologic investigations on 33 retrieved nobelpharma implants. Clin Mater. 1993;12(1):1–9. 5. Cochran DL, Hermann JS, Schenk RK, Higginbottom FL, Buser D. Biologic width around titanium implants. A histometric analysis of the implanto-gingival junction around unloaded and loaded nonsubmerged implants in the canine mandible. J Periodontol. 1997;68(2):186–98. 6. Ericsson I, Lindhe J. Probing depth at implants and teeth. An experimental study in the dog. J Clin Periodontol. 1993;20(9):623–7. 7. Schou S, Holmstrup P, Stoltze K, Hjorting-Hansen E, Fiehn NE, Skovgaard LT.  Probing around implants and teeth with healthy or inflamed peri-implant mucosa/gingiva. A histologic comparison in cynomolgus monkeys (Macaca fascicularis). Clin Oral Implants Res. 2002;13(2):113–26. 8. Khan A, Sharma D. Management of peri-implant diseases: a survey of Australian periodontists. Dent J (Basel). 2020;8(3):100. 9. Berglundh T, Armitage G, Araujo MG, Avila-Ortiz G, Blanco J, Camargo PM, et  al. Peri-­ implant diseases and conditions: consensus report of workgroup 4 of the 2017 world workshop on the classification of periodontal and Peri-implant diseases and conditions. J Clin Periodontol. 2018;45(Suppl 20):S286–S91. 10. Jafarzadeh H, Sanatkhani M, Mohtasham N. Oral pyogenic granuloma: a review. J Oral Sci. 2006;48(4):167–75. 11. Scully C, Eisen D, Carrozzo M.  Management of oral lichen planus. Am J Clin Dermatol. 2000;1(5):287–306. 12. Heitz-Mayfield LJ.  Peri-implant diseases: diagnosis and risk indicators. J Clin Periodontol. 2008;35(8 Suppl):292–304. 13. Karbach J, Callaway A, Kwon YD, d'Hoedt B, Al-Nawas B. Comparison of five parameters as risk factors for peri-mucositis. Int J Oral Maxillofac Implants. 2009;24(3):491–6. 14. Roos-Jansaker AM, Renvert H, Lindahl C, Renvert S.  Nine- to fourteen-year follow-up of implant treatment. Part III: factors associated with peri-implant lesions. J Clin Periodontol. 2006;33(4):296–301. 15. Ferreira SD, Silva GL, Cortelli JR, Costa JE, Costa FO. Prevalence and risk variables for peri-­ implant disease in Brazilian subjects. J Clin Periodontol. 2006;33(12):929–35. 16. Ferreira CF, Buttendorf AR, de Souza JG, Dalago H, Guenther SF, Bianchini MA. Prevalence of peri-implant diseases: analyses of associated factors. Eur J Prosthodont Restor Dent. 2015;23(4):199–206. 17. Heitz-Mayfield LJA, Salvi GE.  Peri-implant mucositis. J Periodontol. 2018;89(Suppl 1):S257–S66. 18. Schwarz F, Derks J, Monje A, Wang HL. Peri-implantitis. J Clin Periodontol. 2018;45(Suppl 20):S246–S66. 19. Figuero E, Graziani F, Sanz I, Herrera D, Sanz M. Management of peri-implant mucositis and peri-implantitis. Periodontol 2000. 2014;66(1):255–73. 20. Renvert S, Polyzois I, Maguire R. Re-osseointegration on previously contaminated surfaces: a systematic review. Clin Oral Implants Res. 2009;20(Suppl 4):216–27. 21. Renvert S, Aghazadeh A, Hallstrom H, Persson GR. Factors related to peri-implantitis—a retrospective study. Clin Oral Implants Res. 2014;25(4):522–9.

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22. Alqahtani F, Alqahtani M, Shafqat SS, Akram Z, Al-Kheraif AA, Javed F. Efficacy of mechanical debridement with adjunctive probiotic therapy in the treatment of peri-implant mucositis in cigarette-smokers and never-smokers. Clin Implant Dent Relat Res. 2019;21(4):734–40. 23. Alqahtani F, Alqhtani N, Alkhtani F, Divakar DD, Al-Kheraif AA, Javed F. Efficacy of mechanical debridement with and without adjunct antimicrobial photodynamic therapy in the treatment of peri-implantitis among moderate cigarette-smokers and waterpipe-users. Photodiagn Photodyn Ther. 2019;28:153–8. 24. Javed F, BinShabaib MS, Alharthi SS, Qadri T. Role of mechanical curettage with and without adjunct antimicrobial photodynamic therapy in the treatment of peri-implant mucositis in cigarette smokers: a randomized controlled clinical trial. Photodiagn Photodyn Ther. 2017;18:331–4. 25. Romanos GE, Javed F, Delgado-Ruiz RA, Calvo-Guirado JL. Peri-implant diseases: a review of treatment interventions. Dent Clin N Am. 2015;59(1):157–78. 26. Javed F, Romanos GE. Does photodynamic therapy enhance standard antibacterial therapy in dentistry? Photomed Laser Surg. 2013;31(11):512–8. 27. Javed F, Al Amri MD, Kellesarian SV, Al-Askar M, Al-Kheraif AA, Romanos GE. Laminin coatings on implant surfaces promote osseointegration: fact or fiction? Arch Oral Biol. 2016;68:153–61. 28. Ahmed P, Bukhari IA, Albaijan R, Sheikh SA, Vohra F. The effectiveness of photodynamic and antibiotic gel therapy as an adjunct to mechanical debridement in the treatment of peri-­ implantitis among diabetic patients. Photodiagn Photodyn Ther. 2020;32:102077. 29. Albaker AM, ArRejaie AS, Alrabiah M, Abduljabbar T.  Effect of photodynamic and laser therapy in the treatment of peri-implant mucositis: a systematic review. Photodiagn Photodyn Ther. 2018;21:147–52. 30. Chambrone L, Wang HL, Romanos GE. Antimicrobial photodynamic therapy for the treatment of periodontitis and peri-implantitis: an American Academy of periodontology best evidence review. J Periodontol. 2018;89(7):783–803. 31. Romeo U, Nardi GM, Libotte F, Sabatini S, Palaia G, Grassi FR. The antimicrobial photodynamic therapy in the treatment of peri-implantitis. Int J Dent. 2016;2016:7692387. 32. van Winkelhoff AJ.  Antibiotics in the treatment of peri-implantitis. Eur J Oral Implantol. 2012;5(Suppl):S43–50. 33. Al-Hamoudi N. Is antimicrobial photodynamic therapy an effective treatment for chronic periodontitis in diabetes mellitus and cigarette smokers: a systematic review and meta-analysis. Photodiagn Photodyn Ther. 2017;19:375–82. 34. Al Hafez ASS, Ingle N, Alshayeb AA, Tashery HM, Alqarni AAM, Alshamrani SH.  Effectiveness of mechanical debridement with and without adjunct antimicrobial photodynamic for treating peri-implant mucositis among prediabetic cigarette-smokers and non-­ smokers. Photodiagn Photodyn Ther. 2020;31:101912. 35. Adell R, Lekholm U, Rockler B, Branemark PI, Lindhe J, Eriksson B, et al. Marginal tissue reactions at osseointegrated titanium fixtures (I). A 3-year longitudinal prospective study. Int J Oral Maxillofac Surg. 1986;15(1):39–52. 36. Zarb GA, Schmitt A.  The longitudinal clinical effectiveness of osseointegrated dental implants: the Toronto study. Part III: problems and complications encountered. J Prosthet Dent. 1990;64(2):185–94. 37. Marquez IC. The role of keratinized tissue and attached gingiva in maintaining periodontal/ peri-implant health. Gen Dent. 2004;52(1):74–8; quiz 9. 38. Kim BS, Kim YK, Yun PY, Yi YJ, Lee HJ, Kim SG, et al. Evaluation of peri-implant tissue response according to the presence of keratinized mucosa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;107(3):e24–8. 39. Bouri A Jr, Bissada N, Al-Zahrani MS, Faddoul F, Nouneh I.  Width of keratinized gingiva and the health status of the supporting tissues around dental implants. Int J Oral Maxillofac Implants. 2008;23(2):323–6.

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40. Lang NP, Mombelli A, Tonetti MS, Bragger U, Hammerle CH. Clinical trials on therapies for peri-implant infections. Ann Periodontol. 1997;2(1):343–56. 41. Persson LG, Ericsson I, Berglundh T, Lindhe J. Guided bone regeneration in the treatment of periimplantitis. Clin Oral Implants Res. 1996;7(4):366–72. 42. Ericsson I, Persson LG, Berglundh T, Edlund T, Lindhe J. The effect of antimicrobial therapy on periimplantitis lesions. An experimental study in the dog. Clin Oral Implants Res. 1996;7(4):320–8. 43. Froum SJ, Froum SH, Rosen PS. A regenerative approach to the successful treatment of Peri-­ implantitis: a consecutive series of 170 implants in 100 patients with 2- to 10-year follow-up. Int J Periodontics Restorative Dent. 2015;35(6):857–63. 44. Roy M, Loutan L, Garavaglia G, Hashim D. Removal of osseointegrated dental implants: a systematic review of explantation techniques. Clin Oral Investig. 2020;24(1):47–60. 45. Zitzmann NU, Berglundh T.  Definition and prevalence of peri-implant diseases. J Clin Periodontol. 2008;35(8 Suppl):286–91. 46. Lindhe J, Meyle J, Group DoEWoP.  Peri-implant diseases: consensus report of the sixth European workshop on periodontology. J Clin Periodontol. 2008;35(8 Suppl):282–5. 47. Dixon DR, London RM.  Restorative design and associated risks for peri-implant diseases. Periodontol 2000. 2019;81(1):167–78. 48. Korsch M, Walther W, Bartols A. Cement-associated peri-implant mucositis. A 1-year follow­up after excess cement removal on the peri-implant tissue of dental implants. Clin Implant Dent Relat Res. 2017;19(3):523–9. 49. Yue ZG, Zhang HD, Yang JW, Hou JX. Comparison of residual cement between CAD/CAM customized abutments and stock abutments via digital measurement in vitro. Beijing Da Xue Xue Bao. 2020;53(1):69–75. 50. Thoma DS, Naenni N, Figuero E, Hammerle CHF, Schwarz F, Jung RE, et al. Effects of soft tissue augmentation procedures on peri-implant health or disease: a systematic review and meta-analysis. Clin Oral Implants Res. 2018;29(Suppl 15):32–49. 51. Heitz-Mayfield LJA, Salvi GE, Mombelli A, Loup PJ, Heitz F, Kruger E, et al. Supportive peri-­ implant therapy following anti-infective surgical peri-implantitis treatment: 5-year survival and success. Clin Oral Implants Res. 2018;29(1):1–6. 52. Costa FO, Takenaka-Martinez S, Cota LO, Ferreira SD, Silva GL, Costa JE.  Peri-implant disease in subjects with and without preventive maintenance: a 5-year follow-up. J Clin Periodontol. 2012;39(2):173–81. 53. Olmedo DG, Paparella ML, Brandizzi D, Cabrini RL. Reactive lesions of peri-implant mucosa associated with titanium dental implants: a report of 2 cases. Int J Oral Maxillofac Surg. 2010;39(5):503–7. 54. Buchner A, Shnaiderman-Shapiro A, Vered M. Relative frequency of localized reactive hyperplastic lesions of the gingiva: a retrospective study of 1675 cases from Israel. J Oral Pathol Med. 2010;39(8):631–8. 55. Al-Khateeb TH. Benign oral masses in a northern Jordanian population-a retrospective study. Open Dent J. 2009;3:147–53. 56. Dojcinovic I, Richter M, Lombardi T. Occurrence of a pyogenic granuloma in relation to a dental implant. J Oral Maxillofac Surg. 2010;68(8):1874–6. 57. Etoz OA, Soylu E, Kilic K, Gunhan O, Akcay H, Alkan A. A reactive lesion (pyogenic granuloma) associated with dental implant: a case report. J Oral Implantol. 2013;39(6):733–6. 58. Gorpas D, Davari P, Bec J, Fung MA, Marcu L, Farwell DG, et al. Time-resolved fluorescence spectroscopy for the diagnosis of oral lichen planus. Clin Exp Dermatol. 2018;43(5):546–52. 59. Nosratzehi T. Oral lichen planus: an overview of potential risk factors, biomarkers and treatments. Asian Pac J Cancer Prev. 2018;19(5):1161–7. 60. Anitua E, Pinas L, Escuer-Artero V, Fernandez RS, Alkhraisat MH.  Short dental implants in patients with oral lichen planus: a long-term follow-up. Br J Oral Maxillofac Surg. 2018;56(3):216–20. 61. Thongprasom K. Oral lichen planus: challenge and management. Oral Dis. 2018;24(1–2):172–3.

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62. Arduino PG, Campolongo MG, Sciannameo V, Conrotto D, Gambino A, Cabras M, et  al. Randomized, placebo-controlled, double-blind trial of clobetasol propionate 0.05% in the treatment of oral lichen planus. Oral Dis. 2018;24(5):772–7. 63. Chiang CP, Yu-Fong Chang J, Wang YP, Wu YH, Lu SY, Sun A. Oral lichen planus—differential diagnoses, serum autoantibodies, hematinic deficiencies, and management. J Formos Med Assoc. 2018;117(9):756–65. 64. Agha-Hosseini F, Rohani B.  Evaluation of the effects of dental implants on oral lesions. J Contemp Dent Pract. 2015;16(5):400–6. 65. Pons-Fuster A, Jornet PL.  Dental implants in patients with oral lichen planus: a narrative review. Quintessence Int. 2014;45(7):599–603. 66. Petruzzi M, De Benedittis M, Cortelazzi R, Milillo L, Lucchese A, Serpico R, et  al. Implant rehabilitation in patients with oral lichen planus: an overview. Clin Oral Investig. 2012;16(5):1347–52. 67. Mostafa B, Zakaria M. Evaluation of combined topical ozone and steroid therapy in management of oral lichen planus. Open Access Maced J Med Sci. 2018;6(5):879–84. 68. Hoseinpour Jajarm H, Asadi R, Bardideh E, Shafaee H, Khazaei Y, Emadzadeh M. The effects of photodynamic and low-level laser therapy for treatment of oral lichen planus-a systematic review and meta-analysis. Photodiagn Photodyn Ther. 2018;23:254–60. 69. Scully C, Carrozzo M.  Oral mucosal disease: lichen planus. Br J Oral Maxillofac Surg. 2008;46(1):15–21. 70. Aboushelib MN, Elsafi MH.  Clinical management protocol for dental implants inserted in patients with active lichen planus. J Prosthodont. 2017;26(1):29–33.

7

Prosthetic Role in Peri-Implant Soft Tissue Management: Treatment Planning Phase Mohamed Moataz Khamis

7.1 Introduction Loss of teeth is always associated with loss of alveolar bone and soft tissue. Functional and esthetic restoration of missing teeth necessitates not only tooth restoration (white esthetics) but restoration of lost bone and soft tissue (pink esthetics). Despite the different prosthetic options, dental implants are currently among the best to restore missing teeth because of the many advantages they provide. Dental implant treatment involves the coordination of a team of multiple specialists, including prosthodontists, periodontists, surgeons, and dental technicians. Prosthodontists are supposedly the first of the team members to meet and select proper candidates from those who seek prosthetic restoration of their missing teeth. They should be able, through a well-organized treatment plan, to determine, together with the help of the other team members, the potential candidates for a successful implant treatment. The demand for esthetic implant restorations raises the question of whether the final esthetic result is totally dependent on prosthetic procedures or whether there is a need for surgical intervention and reconstruction. An additional concern is how far can prosthetics contribute to peri-implant soft tissue management and esthetics. Tooth restoration or white esthetics can totally be achieved by prosthetic techniques and procedures through the construction of a restoration having proper tooth shape, shade, size, position, and alignment. However, soft tissue or pink esthetics can be achieved by a combination of surgical and prosthetic techniques. The surgical role involves proper implant positioning, together with bone and soft tissue augmentation and management. In contrast, the prosthetic role involves many steps that have a direct impact on the final soft tissue outcome.

M. M. Khamis (*) Department of Prosthodontics, Faculty of Dentistry, Alexandria University, Alexandria, Egypt © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_7

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Although the surgical role is the main player in soft tissue reconstruction and management, prosthetics can sometimes solve problems that are difficult to manage surgically and can augment the surgical procedures to reach satisfactory results. It is therefore imperative to highlight how prosthetics can contribute to soft tissue management and health around implants to promote an effective collaboration between the different specialty team members.

7.2 Patient Selection The first step in implant treatment is the proper selection of potentially successful candidates for implant restorations. Although the first specialty to choose potential candidates are usually prosthodontists, a consultation with the surgeon and/or periodontist is highly recommended, especially if peri-implant soft tissue management is necessary. Patient selection involves many considerations involving prosthetic, surgical, psychological, and financial issues. However, regarding soft tissue management, specific points should be considered.

7.2.1 Amount of Soft Tissue Showing During Smiling Restoring peri-implant hard and soft tissues can be performed for functional and/or esthetic reasons. In the esthetic zone, the amount of soft tissue showing during smiling determines whether treatment planning should be geared toward a functional or esthetic protocol. In the case of an esthetic protocol, a combination of surgical and prosthetic approaches should be implemented. According to Johnson [1], alveolar bone resorbs and loses about 25% of its volume during the first year and up to 40–60% in width within the first 3 years of tooth loss. Schropp et al. [2] reported that as much as 40% to 50% of alveolar width and 20% to 30% of height are irreversibly lost during the first year following extraction. Most of the dimensional alterations of the alveolar ridge, whether horizontal or vertical, take place during the first 3 months of healing [3]. This implies that patients seeking tooth restoration, especially those with a high smile line in the esthetic zone following a few months of tooth extraction, would likely require both surgical (bone and/or soft tissue grafting) and prosthetic approaches (Fig. 7.1). Fig. 7.1  Soft tissue defect requiring surgical and prosthetic approaches for correction

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7.2.2 Understanding Patient Demands and Expectations Understanding patient expectations of the final prosthetic result, especially the esthetic part, is sometimes a difficult task. Lack of consideration of patient expectations might result in an unsatisfied patient. In patients with low lip lines or when soft tissues do not show during smiling, treatment planning is usually directed toward functionally restoring teeth, concentrating on white esthetics, and not necessarily restoring pink esthetics if their deficiency is not compromising functional implant positioning. Restoring conditions with bone and soft tissue defects without augmentation usually results in restorations that are longer occluso-cervically than their neighboring counterparts. In most of the cases, this does not cause an esthetic problem as it does not show during smiling (Fig. 7.2a, b). Adding a pink-colored section to the restoration (commonly gingival porcelain) can sometimes be used to improve the esthetic outcome (Fig. 7.3). However, it is important to understand the patient’s demands and expectations. Even though they do not show during smiling, some patients still psychologically prefer bone and soft tissue augmentation to naturally restore their soft tissue defects (Fig. 7.4). This must be clear from the start to tailor the treatment plan accordingly.

a

b

Fig. 7.2 (a) Long restoration occluso-cervically due to lack of augmentation of bone and soft tissue defect. (b) Acceptable esthetic result because of the low lip line Fig. 7.3  Adding gingival porcelain of suitable shade to improve the esthetic outcome

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Fig. 7.4  Bone and soft tissue defect requiring a staged grafting procedure. Acceptable prosthetic result following a staged guided bone regeneration procedure

Fig. 7.5  Digital smile design can aid in understanding patient expectations

7.2.3 Digital Smile Design One way of understanding patient expectations is through a digital smile design [4–6], which can be used to fabricate a mockup. This way, an objective decision can be reached based on patient acceptance of the result (Fig.  7.5). After patient

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approval, the digital smile design can be used to fabricate a surgical guide for proper implant placement and soft tissue augmentation. It can also be used to construct a temporary restoration [5, 6].

7.3 Treatment Planning Once an appropriate patient is selected, treatment planning should be performed. Treatment planning involves many considerations, including implant selection, placement techniques, biomechanics, soft tissue management, and prosthetic procedures, all geared the placement of the implant in a proper prosthetic position to reach a final acceptable result. Knowing the capabilities of the team members of different specialties is important to be able to coordinate the efforts to reach optimal results.

7.3.1 Esthetic Implant Positioning The demand for an esthetic implant restoration is always increasing. Patient demands and expectations when implants are used to restore missing teeth are usually very high and in some cases unrealistic. However, to achieve ultimate esthetic results, some considerations need to be addressed, including proper patient selection, implant positioning and alignment, creation of a proper emergence profile, and restoring lost bone and soft tissue. To achieve an acceptable, esthetic peri-implant soft tissue contour, implants should be properly positioned and aligned in three dimensions: mesiodistally, labiolingually, and apicoincisally. In the esthetic zone, implants should be used to restore missing teeth only if they can be placed in a proper prosthetic position or else it would be difficult to combine esthetics together with a hygienic design. To ensure proper positioning and alignment as treatment planned, surgical guides can be fabricated and used. According to the degree of limitation of the surgical guide, guides can be nonlimiting, partially limiting, or completely limiting [7]. Conventional surgical guides are usually nonlimiting. They are mainly intended to guide implant placement from a prosthetic point of view but do not ensure accurate positioning or limit the depth of drilling (Fig. 7.6). They usually guide implant direction. CAD-CAM fabricated guides can be partially or completely limiting. Partially limiting guides control the direction and depth of drilling for the first few drills. The final drill, however, is used free hand guided by the direction of the previous drills (Fig. 7.7). The completely limiting guides control the drilling procedure from the start all the way to implant placement. They therefore guide implant placement prosthetically and surgically as implant depth and relation to important anatomical structures are also controlled [5, 7] (Fig. 7.8). Studies comparing the accuracy of implant placement between partially and fully guided CAD-CAM fabricated surgical guides do not show a clinically

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Fig. 7.6  Nonlimiting conventional surgical guide

Fig. 7.7  Partially limiting guide

significant difference between both techniques [8]. However, one of the concerns of using those guides was the difficulty of the cooling solution to reach the osteotomy site during drilling because of the precision between the drill shank and the guiding holes of the surgical guide. The inability to provide sufficient irrigation during drilling might compromise the peri-implant hard and soft tissues. To improve the efficiency of irrigation and at the same time maintain guidance, C-shaped guide holes can be used (Fig. 7.9). In a study comparing the peri-implant soft and hard tissues

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Fig. 7.8  Completely limiting guide

Fig. 7.9  C-shaped guide holes

after flapless implant placement by using fully guided versus partially guided surgical guides with cylindrical versus C-shaped guide holes, no clinical or radiographic difference was found [9]. Implants can therefore be placed accurately by using CAD-CAM fabricated guides without compromising peri-implant hard and soft tissues [10, 11].

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7.3.2 Submerged Versus Non-submerged Implants Implants can be placed by using a submerged or a non-submerged protocol [12]. Submerged implants can have a short 1  mm or less smooth collar height. Some designs do not have a smooth collar, especially those with platform switching [13]. Non-submerged implant designs have a long smooth collar about 2.5 mm in length (Fig.  7.10). Those implants provide two advantages: first, they are kept non-­ submerged, eliminating the need for a second-stage surgery procedure with all its drawbacks; second, keeping the implant abutment junction (micro gap) supragingival. The implant abutment micro gap has been considered one of the reasons for crestal bone resorption that occurs during the first year following implant placement [14]. Keeping the micro gap away from the bone level might reduce the rate of bone resorption [15, 16]. The drawbacks of using non-submerged implants include the possibility of an unesthetic intraoral metal collar show, especially if peri-implant soft tissue recession occurs (Fig. 7.11). One way to overcome this problem is to use a submerged implant design together with a healing abutment placed at the time of implant insertion. This way, a second-stage procedure is avoided and at the same time a final restoration with a subgingival finish line can be created [12] (Fig. 7.12). The non-submerged implant design should be used in cases when a second-stage procedure is to be avoided in the non-esthetic zone, implants have good primary

Fig. 7.10 Submerged implant design on the left. Non-submerged implant design on the right

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Fig. 7.11 Unesthetic metal collar show as a result of peri-implant soft tissue recession

Fig. 7.12  Submerged implant design with a healing abutment attached at the time of implant placement, making it a single-stage procedure

stability, and preferably when there is no need for guided bone regeneration [12]. To overcome the unesthetic properties of single-stage implants, some companies provide implants with tooth-colored collars or implants totally made of zirconia [17].

7.4 Restoration Emergence Profile The contour of the gingival margin of teeth is an important determinant of an esthetic smile. In spite of the difference in contour of the gingival margin among natural teeth, symmetry between contralateral teeth is essential to ensure uniformity. The contour of the gingival margin of teeth is determined by the facial bone contour, gingival texture, and emergence profile of the individual tooth [18]. The emergence profile of a tooth is its profile while emerging from the gingiva.

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Fig. 7.13  Cross section of natural teeth at the bone level showing the difference between natural teeth cross section and round dental implants

The cross section of every tooth in the dental arch varies at the bone level (Fig. 7.13). The emergence profile and consequently the gingival margin contour therefore differ as they follow the configuration of the emergence profile of the tooth (Fig.  7.14). The cross section of maxillary incisors is usually triangular, canines are rhomboidal, premolars are oval, and molars are trapezoidal (Fig. 7.15). When natural teeth are restored by using crowns, the emergence profile of the crown should be adjusted and designed to simulate the contralateral side, therefore maintaining a proper gingival margin contour. However, when dental implants are used, their cross section at the bone level is round which is different from all natural teeth that are never round (Fig. 7.16). If an implant restoration is designed with a round emergence profile, this will result in a gingival margin that is not symmetrical when compared to the natural contralateral tooth (Fig. 7.17). The clinician should be aware that the emergence profile of an implant restoration should change from round to triangular if an incisor is to be restored or oval if a premolar is to be restored and so on. This way, the gingival margin of the peri-implant mucosa can be properly and symmetrically contoured [19]. Changing the emergence profile of an implant restoration from round to oval should be performed within the distance between the bone level (implant platform)

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Fig. 7.14  Contour of the gingival margin of natural teeth varies from one tooth to another depending on the tooth emergence profile

Fig. 7.15 Difference between the emergence profile of natural teeth and round dental implants

a

b

Fig. 7.16  The round implant cross section should be changed to the natural tooth emergence profile to restore the esthetic peri-implant soft tissue margin (a) proximal view. (b) facial view

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Fig. 7.17 Improperly designed transition between the round implant cross section and the triangular central incisor emergence profile compromising the overall esthetic result

2-3 mm

Fig. 7.18  Emergence profile change from round to triangular, oval, or rhomboidal should be performed within the distance between the implant platform and the peri-implant soft tissue margin

and the gingival margin (Fig.  7.18). An average of 3  mm is required to allow a smooth transition [20]. Proper positioning of the implant occluso-cervically is therefore important to ensure enough space for the creation of the emergence profile. Creation of a proper emergence profile can be performed during most of the steps of implant treatment, including implant selection, implant positioning, flapless placement with a single-stage procedure, second-stage surgery, selection of a healing abutment, temporary crown fabrication, selection of an impression coping, abutment selection, and final prosthesis construction.

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Fig. 7.19  Implants having a flared neck (collar) allow a smooth transition from implant to restoration

7.4.1 Implant Selection Two features of an implant can affect the restoration emergence profile: the form of the implant neck portion and the implant platform diameter.

7.4.1.1 Form of the Neck Portion Some implant designs have a flared implant collar (neck) (Fig. 7.19). Most of these implants are designed to be placed in a single-stage procedure. The flared implant neck allows a smooth transition from the implant to the restoration, resulting in a hygienic profile. 7.4.1.2 Implant Diameter The selection of a proper implant diameter is essential to facilitate a proper emergence profile. An implant diameter that is slightly smaller than the diameter of the neck of a natural tooth (buccolingually and mesiodistally) allows a smooth transition between the implant platform and restoration (Fig. 7.20). An implant diameter that is too narrow makes it difficult to change from a round platform to a triangular or oval one. A sudden or abrupt change would be necessary, making it nonhygienic (Fig. 7.21). An alternative would be to emerge gradually, resulting in mesial and distal black triangles (Fig. 7.22). Too wide diameter is also unacceptable as it leads to an unesthetic restoration. Improper implant diameter selection will therefore result in loss of either esthetics or hygiene. Choosing a narrow diameter is usually associated with reduced buccolingual diameter of the residual bone resulting from delayed restoration and bone resorption. In such cases, the ideal setting is to graft the bone, increasing its width to be able to choose the proper implant diameter. An alternative is to use an implant with a narrow diameter but a wide platform (Fig. 7.23).

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Fig. 7.20  Selection of a proper implant diameter ensures a proper emergence profile Fig. 7.21  Too narrow implant diameter interfering with proper emergence profile

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Fig. 7.22  Too narrow implant diameter resulting in an emergence profile with black mesial and distal triangles

Fig. 7.23  An implant with a narrow diameter and a wide platform can be used in cases having a narrow buccolingual dimension and a wide mesiodistal one

7.4.2 Implant Positioning The best position for an implant is the original tooth position provided that the tooth was in a proper position. An implant is positioned in three dimensions: mesiodistally, buccolingually, and apicoincisally.

7.4.2.1 Labio-Lingual Positioning Maxillary and mandibular anterior implants should be positioned slightly palatal to the long axis of the tooth to be restored (Fig.  7.24). This is mainly to allow a

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b

Fig. 7.24 (a) Long axis of maxillary and mandibular anterior teeth directed slightly palatal to allow the screw access channel to be located at the cingulum area. (b) Implant placed too far palatal, resulting in a short restoration that can be corrected by creating a lap ridge relation

thickness of the restoration on the labial surface to ensure translucency and avoid a thin weak restoration that might show the shadow of the metal abutment in the case of all ceramic restorations interfering with restoration esthetics by giving a grey hue. A slightly palatal position also allows a screw-retained restoration to have a palatally located screw access channel without the need for an angled abutment [20]. The problem exists in cases of delayed restoration after tooth extraction. Extensive labial bone resorption forces implant placement to be performed too far palatal, resulting in a short restoration (Figs. 7.25 and 7.26). To prosthetically correct this situation, a lap ridge relation can be designed to gingivally increase the length of the restoration (Fig. 7.24b) [20]. However, this ends up with an unhygienic emergence profile, resulting in peri-implant soft tissue problems. To avoid a palatal position, bone must be grafted to warrant a proper implant position. An alternative is to position the implant more apical to the ideal position, which should be 2–3 mm apical to the free gingival margin. Placing an implant 1 mm palatal to the idea position should be associated with a 1-mm apical position (Fig. 7.27). Too far labial implant positioning results in a long restoration that cannot be easily corrected. A prosthetic solution would be to add a pink-colored restoration material (gingival porcelain) to the cervical part of the restoration (Fig.  7.28). This requires a talented technician to create an acceptable gingival contour and acceptable tissue shade of the gingival porcelain. In many cases, the implant is removed and a new one is placed in a proper position. To avoid a lap ridge relation, the implant can be placed in an apical position.

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Fig. 7.25  Implant placed too far palatal resulting in a short restoration

7.4.2.2 Mesio-Distal Positioning An implant should be positioned in the mesio-distal center of the tooth to be restored. Improper mesiodistal position results in compromised esthetics and/or hygiene (Fig. 7.29). An implant placed too close to a neighboring tooth will also prosthetically interfere with impression making, abutment attachment, and final restoration contour (Fig. 7.30). When multiple implants are placed, proper mesiodistal implant orientation should be achieved bearing in mind the inter-implant distance as it has a direct effect on the configuration of the interdental papilla. An average distance of 3  mm is required between two adjacent implants to ensure acceptable interdental papilla configuration [21, 22] (Fig. 7.31).

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Fig. 7.26  Implant placed slightly palatal resulting in a slightly short restoration Fig. 7.27  To avoid a lap ridge relation (a), implant can be placed in a more apical position (b)

a

b

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Fig. 7.28  Too far labial implant position results in a long restoration. Tissue-colored restorative material can improve the esthetic result Fig. 7.29 Improper mesiodistal centralization of an implant compromises esthetics and hygiene

7.4.2.3 Apico-Incisal Positioning In the esthetic zone, the ideal implant position should be submerged an average of 2–3 mm apical to the free gingival margin of neighboring teeth to be able to create an acceptable emergence profile (Fig. 7.32) [20]. Too deep apical implant position results in an unhygienic design, similar to a pocket in a natural tooth. Too far incisal positioning will not give a chance for a smooth transition between implant diameter and configuration and tooth design, resulting in a defective emergence profile together with the possibility of an abutment collar show compromising esthetics too. A relation exists between implant diameter and its apico-incisal level of positioning. The more apical the implant position, the narrower the implant diameter to facilitate the creation of an acceptable emergence profile (Fig. 7.33).

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Fig. 7.30 Implant positioned too close to a neighboring tooth interfering with abutment and restoration attachment

Fig. 7.31  An average distance of 3 mm is required between two adjacent implants to ensure an adequate size of interdental papilla

2-4 mm

2-4 mm

Fig. 7.32  A minimum space of 2–3 mm is required between the implant platform and free gingival margin to allow for a properly designed and contoured restoration emergence profile

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Fig. 7.33  The more apical the implant position, the narrower should be the implant diameter

Proper implant position in all three planes therefore has a direct effect on esthetics, biomechanics, phonetics, and hygiene [23–25]. If multiple implants are placed too close to each other, esthetics and hygiene would be compromised while biomechanics and phonetics would not be affected. If neighboring implants were placed too far from each other, esthetics, phonetics, and hygiene would be compromised, while biomechanics would not be affected (Fig. 7.34).

7.4.3 Immediate Implant Placement in a Freshly Extracted Socket by Using a Flapless Single-Stage Procedure Preserving the gingiva, gingival margin, and interdental tissues around natural teeth following extraction is a goal that needs to be achieved. One way to do this is to extract the tooth atraumatically and place the implant flapless [26]. However, to preserve the soft tissue contour, a wide diameter stock healing abutment (Fig. 7.35) or a custom-made one (Fig.  7.36a,b) must be placed immediately at the time of implant placement. Creating a healing abutment with an identical emergence profile to the extracted tooth can aid the soft tissue to heal in a similar way to that around the natural tooth [27]. Multiple techniques are available for custom-made healing abutment fabrication [28, 29]. However, conventional methods require considerable chairside time. In addition, the intraorally polymerized resins used to construct the healing abutments have been reported to release byproducts and free monomers that have a detrimental effect on peri-implant tissues [30]. CAD-CAM technology can

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Esthetics

Biomechanics

Phonetics

Hygiene

Optimal

Too Close

Too Wide

Too Angulated Too Labial/Palatal

Good

Difficult

Great problems

Fig. 7.34  Relation between implant position and esthetics, biomechanics, phonetics, and hygiene

a

c

b

d

Fig. 7.35 (a, b) Stock healing abutment inserted immediately at the time of implant placement. (c, d) Soft tissue healing around stock healing abutments

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Fig. 7.36  Custom-made healing abutments attached to implants at the time of implant placement

nowadays aid in designing and fabrication of custom-made healing abutments. A custom-made healing abutment that duplicates the emergence profile of the tooth being extracted or the tooth on the contralateral side can be fabricated before extraction to be inserted immediately after implant placement [19] (Fig. 7.37a–h). The indirect fabrication avoids residual monomer and improves cell attachment. It also saves chairside time and ultimately patient satisfaction.

7.4.4 Second-Stage Surgery Second-stage surgery can be performed by raising a flap and by using a tissue punch, lasers, and the cross technique. Raising a flap is usually indicated whenever the implant cannot be located or is covered by bone, as in cases of submerging the implant too much during insertion [31]. A tissue punch is a useful option in the non-­ esthetic zone. The drawback of which is that valuable keratinized soft tissue is lost (Fig. 7.38). Dental lasers have improved dramatically in the past few years. By using a dental laser, peri-implant soft tissue can be carved to create an acceptable emergence profile [32, 33]. Again, lasers remove from the soft tissue, which might not be a wise decision in the esthetic zone. However, they can be a useful tool for refining peri-­ implant soft tissue contours and to perform hemostasis, especially if a direct digital impression is to be made [34–38] (Fig. 7.39). To shape the peri-implant soft tissue contour, healing abutments can be placed at the second-stage surgery procedure. Custom-made healing abutments or temporary crowns can also be designed to create a favorable emergence profile that can be altered and modified by adjusting the healing abutment contour until a desirable shape is reached [19, 27]. The final restoration is made later on to duplicate the modified healing abutment.

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a

b2

b1

c

d

Fig. 7.37 (a) Non-restorable tooth, (b1) Segmented tooth (red) with maxillary cast aligned with DICOM file. (b2) Mirrored tooth (blue) in place. (c) Custom healing shell designed. (d) Clinical evaluation of custom healing shell with interim abutment in place. (e) Healing shell attached to the interim abutment. (f) Custom healing abutment in place. (g) Custom healing abutment out of occlusion. (h) Definitive restoration in place

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e

g

Fig. 7.37 (continued) Fig. 7.38  Tissue punch is used to expose the implant during the second-stage surgery procedure

f

h

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Fig. 7.39  Dental laser (Er,Cr:YSGG, Biolase) used to perform the second-stage procedure together with refining peri-implant soft tissue contour

7.4.5 Impression Coping After creating an acceptable emergence profile and soft tissue contour by using a custom-made healing abutment or temporary crown, the soft tissue contour should be copied to the cast sent to the technician to design the final restoration with a similar emergence profile to that of the shaped and contoured soft tissue. Impression copings (transfer copings) can be customized intraorally by adding flowable composite to match the shape of the peri-implant soft tissue [39, 40]. An alternative technique would be to make the impression while the contoured provisional restoration is in place on the implant. The restoration is later unscrewed, and an analog is attached to it and reinserted into the impression that is poured. After unscrewing the provisional restoration, an accurate imprint of the contoured soft tissue is duplicated on the cast [41]. This would help the dental technician to fabricate a restoration with a similar emergence profile to the one that had already been made (Fig. 7.40a–e).

7.4.6 Abutment Selection Stock abutments, whether screw or cement retained, are usually supplied with a round cross-section of different diameters and collar heights. An abutment of appropriate diameter should be selected to match the diameter of the tooth to be restored. This way, a proper emergence profile can be created (Fig. 7.41) [42]. Custom-made abutments can be constructed by using different materials, most commonly tooth-­ colored ones to avoid metal display, especially in cases with a thin peri-implant soft tissue biotype [43]. Custom-made abutments can be constructed by using conventional techniques or CAD-CAM technology. They offer many advantages over stock ones. Most important is the ability to create a custom emergence profile that guides

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a

c

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b

d

e

Fig. 7.40 (a) Provisional restoration after final contouring, (b) Peri-implant soft tissue contoured by the provisional restoration, (c) Impression with the provisional restoration that is unscrewed from the patient mouth, implant analog attached to it and reinserted back into the impression. (d) Impression is poured. Gingival mask material is added, (e) Peri-implant soft tissue profile duplicated on the case

the gingival margin to a proper contour and the ability to create a custom finish line following the contour of the peri-implant soft tissue margin to be able to efficiently remove excess cement (Fig. 7.42a,b).

7.4.7 Final Restoration A well-designed final restoration with a properly contoured emergence profile is essential to support peri-implant soft tissues, thus creating an esthetic gingival margin. Ultimate esthetic results with implants can be achieved by using tooth-colored, metal-free restorations (Fig. 7.43a–d).

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Fig. 7.41 Stock abutments are provided with different diameters selected according to the clinical situation

a

b

Fig. 7.42 (a) Tooth-colored zirconia abutment. (b) Lithium disilicate restoration with appropriate color match

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c

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d

Fig. 7.43 (a) Properly positioned implant, (b) properly contoured peri-implant soft tissue margin by using a contoured conventional restoration, (c) all ceramic (lithium disilicate) final restoration with a suitable emergence profile, and (d) all ceramic (lithium disilicate) final restoration with a suitable emergence profile

References 1. Johnson K. A study of the dimensional changes occurring in the maxilla after tooth extraction. Part I. Normal healing. Aust Dent J. 1963;8:428–33. 2. Schropp L, et al. Bone healing and soft tissue contour changes following single-tooth extraction: a clinical and radiographic 12-month prospective study. Int J Periodontics Restorative Dent. 2003;23(4):313–23. 3. Johnson K.  A study of the dimensional changes occurring in the maxilla following tooth extraction. Aust Dent J. 1969;14:241–4. 4. Cattoni F, Chirico L, Merlone A, Manacorda M, Vinci R, Gherlone EF. Digital smile designed computer-aided surgery versus traditional workflow in "all on four" rehabilitations: a randomized clinical trial with 4-years follow-up. Int J Environ Res Public Health. 2021;18(7):3449. https://doi.org/10.3390/ijerph18073449. PMID: 33810379; PMCID: PMC8037328. 5. Ramadan RE, Bahgat MM, Abdelhamid AM, Khamis MM.  Registration of maxillomandibular relationship through a fully digital workflow for complete-mouth rehabilitation with screw-retained fixed implant-supported prostheses: a clinical report. J Prosthet Dent. 2023;S0022-3913(22):00760. https://doi.org/10.1016/j.prosdent.2022.11.027. 6. Gadallah MA, Aboelsayed KM, Neena AF, Khamis MM. Digitally empowered esthetic dentistry “functionally and biologically driven digital smile design”. Alex Dent J. 2023;47:24. https://doi.org/10.21608/adjalexu.2023.273772.

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7. D’Souza KM, Aras MA.  Types of implant surgical guides in dentistry: a review. J Oral Implantol. 2012;38:643–52. 8. Sarhan MM, Khamis MM, El-Sharkawy AM. Evaluation of the accuracy of implant placement by using fully guided versus partially guided tissue supported surgical guides with cylindrical versus C-shaped guiding holes: a split-mouth clinical study. J Prosthet Dent. 2021;125:620–7. 9. Elkomy MM, Khamis MM, El-Sharkawy AM. Clinical and radiographic evaluation of implants placed with fully guided versus partially guided tissue-supported surgical guides: a split mouth clinical study. J Prosthet Dent. 2021;126:58–66. 10. Kammoun YA, Khamis MM, El-Sharkawy AM, Fahmy RA.  Radiographic assessment of bone level changes around four implants supporting immediately loaded mandibular screw-retained prosthesis. Alex Dent J. 2022;47:113. https://doi.org/10.21608/ ADJALEXU.2021.47381.1114. 11. Mohamed LA, Khamis MM, El-Sharkawy AM, Fahmy RA. Evaluation of immediately loaded mandibular four vertical versus tilted posterior implants supporting fixed detachable restorations without versus with posterior cantilevers. Oral Maxillofac Surg. 2022;26:373–81. 12. Buser D, Mericske-Stern R, Dula K, Lang NP.  Clinical experience with one-stage, non-­ submerged dental implants. Adv Dent Res. 1999;13:153–61. https://doi.org/10.117 7/08959374990130010501. 13. Macedo JP, Pereira J, Vahey BR, Henriques B, Benfatti CAM, Magini RS, López-López J, Souza JCM. Morse taper dental implants and platform switching: the new paradigm in oral implantology. Eur J Dent. 2016;10(1):148–54. https://doi.org/10.4103/1305-­7456.175677. PMID: 27011755; PMCID: PMC4784146. 14. Todescan FF, et al. Influence of the microgap in the peri-implant hard and soft tissues: a histomorphometric study in dogs. Int J Oral Maxillofac Implants. 2002;17:467–72. 15. Liu Y, Wang J.  Influences of microgap and micromotion of implant-abutment interface on marginal bone loss around implant neck. Arch Oral Biol. 2017;83:153–60. 16. King GN, Hermann JS, Schoolfield JD, Buser D, Cochran DL. Influence of the size of the microgap on crestal bone levels in non-submerged dental implants: a radiographic study in the canine mandible. J Periodontol. 2002;73:1111–7. 17. Roehling S, Schlegel KA, Woelfler H, Gahlert M.  Zirconia compared to titanium dental implants in preclinical studies-a systematic review and meta-analysis. Clin Oral Implants Res. 2019;30(5):365–95. https://doi.org/10.1111/clr.13425. Epub 2019 Apr 16. 18. Chu SJ, Kan JY, Lee EA, Lin GH, Jahangiri L, Nevins M, Wang HL. Restorative emergence profile for single-tooth implants in healthy periodontal patients: clinical guidelines and decision-making strategies. Int J Periodontics Restorative Dent. 2019;40:19–29. https://doi. org/10.11607/prd.3697. 19. El-Danasory MB, Khamis MM, Hakim AAA, Fahmy RA. CAD-CAM custom healing abutments: a dental technique. J Prosthet Dent. 2022;S0022–3913:00638. https://doi.org/10.1016/j. prosdent.2022.09.019. 20. Engelman MJ. Clinical decision making and treatment planning in osseointegration. Batavia, IL: Quintessence Publishing; 1996. 21. Al-Harbi SA. Nonsurgical management of interdental papilla associated with multiple maxillary anterior implants: a clinical report. J Prosthet Dent. 2005;93:212–6. 22. Tarnow DP, Magner AW, Fletcher P. The effect of the distance from the contact point to the crest of bone on the presence or absence of the interproximal dental papilla. J Periodontol. 1992;63(12):995–6. https://doi.org/10.1902/jop.1992.63.12.995. 23. Sailer I, Karasan D, Todorovic A, Ligoutsikou M, Pjetursson BE. Prosthetic failures in dental implant therapy. Periodontol 2000. 2022;88(1):130–44. https://doi.org/10.1111/prd.12416. PMID: 35103329; PMCID: PMC9305548. 24. Ramanauskaite A, Sader R.  Esthetic complications in implant dentistry. Periodontol 2000. 2022;88(1):73–85. https://doi.org/10.1111/prd.12412. 25. Esquivel J, Meda RG, Blatz MB.  The impact of 3D implant position on emergence profile design. Int J Periodontics Restorative Dent. 2021;41(1):79–86. https://doi.org/10.11607/ prd.5126.

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26. Bhola M, Neely AL, Kolhatkar S.  Immediate implant placement: clinical decisions, advantages, and disadvantages. J Prosthodont. 2008;17(7):576–81. https://doi.org/10.1111/ j.1532-­849X.2008.00359.x. Epub 2008 Aug 26. 27. Chu SJ, Salama MA, Salama H, Garber DA, Saito H, Sarnachiaro GO, Tarnow DP. The dual-­ zone therapeutic concept of managing immediate implant placement and provisional restoration in anterior extraction sockets. Compend Contin Educ Dent. 2012;33(524–532):534. 28. Ruales-Carrera E, Pauletto P, Apaza-Bedoya K, Volpato CA, Özcan M, Benfatti CA.  Peri-­ implant tissue management after immediate implant placement using a customized healing abutment. J Esthet Restor Dent. 2019;31:533e541. 29. Akin R. A new concept in maintaining the emergence profile in immediate posterior implant placement: the anatomic harmony abutment. J Oral Maxillofac Surg. 2016;74:2385e2392. 30. Campaner M, Takamiya AS, Bitencourt SB, et al. Cytotoxicity and inflammatory response of different types of provisional restorative materials. Arch Oral Biol. 2020;111:104643. 31. Linkevicius T, Puisys A, Linkevicius R, Alkimaviciu J, Ginevici E, Limnhevicicene L. The influence of submerged healing abutment or subcrestal implant placement on soft tissue thickness and crestal bone stability. A 2-year randomized clinical trial. Clin Implant Dent Relat Res. 2020;22:497–506. 32. Schuler DE. Use of the laser in the oral cavity. Otolaryngol Clin N Am. 1990;23:31–42. 33. Khamis MM, Abdelrehim AA. Interdisciplinary management of a patient with a gummy smile. J Oral Maxillofac Radiol. 2019;7:38–43. 34. Rizoiu, et al. Effects of an erbium, chromium: yttrium, scandium, gallium, garnet laser on mucocutaneous soft tissues. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996;82:386–95. 35. Tunc SK, Yayli NZ, Talmac AC, Feslihan E, Akbal D.  Clinical comparison of the use of ER,CR:YSGG and diode lasers in second stage implants surgery. Saudi Med J. 2019;40(5):490–8. https://doi.org/10.15537/smj.2019.5.24105. PMID: 31056627; PMCID: PMC6535160. 36. Ramadan RE, Segan L, Abdelhamid AM, Khamis MM.  Gingival melanin depigmentation with 4 different laser wavelengths 445, 940, 1064 and 2940nm: a case report. Alex Dent J. 2022;47:27. https://doi.org/10.21608/adjalexu.2023.273862. 37. Ashry A, Khamis MM, Abdelhamid AM, Segaan LG. Lip repositioning and guided gingivectomy combined treatment for excessive gingival display by using 940-nm diode laser: a case report. Laser Dent Sci. 2023;7:25. https://doi.org/10.1007/s41547-­023-­00174-­5. 38. Troedhan A, Mahmoud ZT, Wainwright M, Khamis MM. Cutting bone with drills, burs, lasers and piezotomes: a comprehensive systematic review and recommendations for the clinician. Int J Oral Craniofac Sci. 2017;3(2):020–33. https://doi.org/10.17352/2455-­4634.0000128. 39. Buskin R, Salinas TJ. Transferring emergence profile created from the provisional to the definitive restoration. Pract Periodontics Aesthet Dent. 1998;10:1171–9. 40. Stumpel J, Haechler W, Bedrossian E.  Customized abutments to shape and transfer peri-­ implant soft-tissue contours. J Calif Dent Assoc. 2000;28:301–9. 41. Tsai BY.  A method for obtaining peri-implant soft-tissue contours by using screw-­ retained provisional restorations as impression copings: a clinical report. J Oral Implantol. 2011;37(5):605–9. 42. Khamis MM, Zakaria NH. Effect of screw access channel on fracture resistance of lithium disilicate cement retained implant supported posterior crowns. J Prosthet Dent. 2022;127:618–25. 43. Farrag KM, Khamis MM. Effect of anodized abutment collars on peri-implant soft tissue: a split-mouth clinical study. J Prosthet Dent. 2021;130(1):59–67.

8

Prosthetic Role in Peri-implant Soft Tissue Management: Prosthetic Phase Mohamed Moataz Khamis

8.1 Restoration Design (Screw Vs. Cement Retention) Fixed implant restorations can either be screw or cement retained (Fig. 8.1). Each design has its merits and drawbacks. Screw-retained restorations are retrievable. Retightening a loose abutment screw can therefore be performed easily. They do not depend on cement for retention. Therefore, the problem of removing excess cement

Fig. 8.1  Fixed implant restorations can either be screw or cement retained

M. M. Khamis (*) Department of Prosthodontics, Faculty of Dentistry, Alexandria University, Alexandria, Egypt © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_8

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Fig. 8.2  Screw access channels can interfere with occlusal contacts

does not exist. However, they require special technical skills and are usually more expensive than cement-retained restorations as they may require additional components and procedures [1]. Cement-retained restorations do not have a screw access channel; therefore, they are more esthetic and provide better occlusal anatomy contacts (Fig. 8.2). They are usually easier to fabricate especially if ready-made stock abutments are used. When multiple cement-retained restorations are used, passivity becomes an advantage. The presence of a cement gap space, the amount of which can be controlled, ensures passivity of the restoration, which is important to avoid undue stresses on implants when abutment screws are tightened [1]. However, if excess cement is not completely removed, adverse peri-implant soft tissue reactions can occur [2]. The choice between screw and cement retention depends on many factors, including interocclusal distance, location of the screw access channel, esthetic demands, need for restoration retrievability, frequency of screw loosening, laboratory efficiency, need for passivity of fit, combining natural tooth and implant support, and finish line location [3–6]. It is important to mention that the choice between using a screw- or cement-­ retained restoration should be decided during the treatment plan phase and not after implant placement. Most of the factors of choice between both designs can be determined during treatment planning. Therefore, the restoration design and means of retention are always predetermined, and the treatment plan and implant positioning and alignment are always geared toward achieving a predictable restoration.

8.1.1 Interocclusal Distance The bond strength of cement retention depends on several factors, the most important being the surface area for cement bonding [7, 8]. The larger the surface of the abutment, the greater the bond strength between the abutment and restoration.

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Fig. 8.3 Manufacturers recommend a minimum inter-arch distance for screw-retained abutments that should be checked during treatment planning

Minimum 6.7 mm

Generally, in cases with a wide inter-arch distance allowing for a longer abutment, screw and cement retention are equally acceptable. However, in cases with narrow inter-arch distance, screw retention is more favorable as it depends on the tightness of the abutment/restoration screw rather than abutment surface area [3, 9]. Unlike cement-retained abutments, those for screw retention usually cannot be modified or shortened. Interarch distance should therefore be measured, and the minimal height of a screw-retained abutment should be selected according to manufacturer guidelines (Fig. 8.3).

8.1.2 Location of the Screw Access Channel Screw-retained restorations require a screw access channel that should be located on the palatal surface of anterior teeth (Fig. 8.4) and in the center of the occlusal surface of posterior teeth (Fig. 8.5) so as not to interfere with the esthetic and biomechanical qualities of the restoration. Screw access channels are usually blocked with the composite resin of a similar shade to the restoration (Fig. 8.6). However, the shade of the composite does not always match the shade of the restoration, especially if the restoration has a metal component, such as porcelain fused to metal. The shadow of the metal usually interferes with the esthetic qualities of the restoration (Fig. 8.7). Locating a screw access channel on an incisal edge or a functional cusp tip might weaken the restoration and therefore should be avoided (Fig. 8.8). This requires implants to be properly aligned during placement to ensure a favorable access hole location. An alternative would be to use angled screw-­ retained abutments or cement-retained restorations that do not have a screw access channel on the final restoration.

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Fig. 8.4  Screw access channel ideally located on the palatal surface of anterior teeth Fig. 8.5  Screw access channel ideally located in the center of the occlusal surface of posterior teeth

Fig. 8.6  Screw access channel blocked with composite resin

8  Prosthetic Role in Peri-implant Soft Tissue Management: Prosthetic Phase Fig. 8.7  The shadow of the metal appearing through the composite interfering with the esthetic qualities of the restoration

Fig. 8.8  Screw access channel should not be located on an incisal edge or a functional cusp so as not to weaken the restoration

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8.1.3 Abutment/Restoration Finish Line Position Abutment/restoration finish line location can either be supragingival, subgingival, or equigingival. Supragingival finish lines have many advantages. They are easier during impression making as there would be no need for soft tissue retraction that might compromise peri-implant soft tissue attachment [10, 11]. Peri-implant soft tissue does not collapse between visits if a temporary restoration is not used, finish line visibility makes lab work procedures simpler, detection of restoration abutment marginal fit is more predictable, and excess cement can easily be removed. The main drawback of supragingival finish lines is the unesthetic appearance of the abutment collar especially if a metal abutment is used (Fig. 8.9). For cement-retained restorations, excess cement can be completely removed without any residues that may compromise the peri-implant soft tissue health. Even for screw-retained restorations, supragingival finish lines are preferable from a biological point of view. A micro gap always exists at the abutment restoration junction, the amount of which varies depending on the technique and accuracy of prosthesis construction [12]. A micro gap of considerable size that may result from a restoration with inaccurate margins can harbor bacteria that may cause

Fig. 8.9  Supragingival finish lines are inappropriate in the esthetic zone, especially with metal abutments

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peri-­implant soft tissue problems. Supragingival location of the micro gap is therefore desirable. When selecting a supragingival finish line, both designs would be similar from a biological point of view. To reduce the amount of micro gap between prosthetic components, it is always recommended to torque the abutment screw according to manufacturer’s instructions by using a torque wrench. According to studies, this significantly reduces the micro gap and consequently peri-implant soft tissue problems [13]. Subgingival finish lines are mainly indicated in the esthetic zone to avoid abutment collar display that can compromise esthetics, especially if a metal abutment is used. In such cases, the subgingival depth of the finish line must be controlled to avoid peri-implant soft and hard tissue problems.

8.1.3.1 Cement-Retained Restorations with a Screw Access Channel Cement-retained restorations have many advantages; however, the difficulty encountered in the complete removal of excess cement precludes their routine use. To solve the problem of excess cement, a modified cement-retained restoration was advocated combining the advantages of screw and cement retention [14]. The modification involves the creation of a screw access channel on the occlusal surface of the cement-retained restoration (Fig.  8.10). After complete intraoral cementation (Fig. 8.11), the restoration/abutment assembly can be removed by unscrewing the abutment screw through the screw access channel and the excess cement can be completely removed extra orally (Fig. 8.12a–c). The restoration after cementation becomes permanently attached to the abutment and can be screw retained onto the implant. The screw access channel can later on be filled with a composite of similar shade [1] (Fig. 8.13a,b). The advantage of this design is that it combines the benefits of both screw and cement retention. The limitations, however, include that it is not recommended if Fig. 8.10  Screw access channel on the occlusal surface of the restoration

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Fig. 8.11 Restoration cemented on abutment by using light cure resin cement

Fig. 8.12  Restoration unscrewed after cementation and excess cement completely removed

the screw access channel is not in a favorable position from an esthetic or biomechanical point of view (Fig. 8.14). Studies have been conducted to evaluate the effect of creating a screw access channel on the structural durability and the fracture resistance of the restoration. Different restorative materials were tested, including zirconia, lithium disilicate, and porcelain fused to metal [1, 15–17]. In spite of the variability of the results between various studies and tested materials, most of the studies did not show

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Fig. 8.13  Screw access channel closed with composite resin of appropriate shade Fig. 8.14  Screw access channel should not be created on the labial or buccal surface of teeth, especially in the esthetic zone

significant weakening of the restorations. In multiunit restorations where passivity of the restoration is of utmost importance, this technique can also be applied provided that implants are parallel or very close to being parallel [18–20] (Fig. 8.15a,b).

8.1.3.2 Peri-implant Soft Tissue Thickness/Finish Line Location Locating the finish line in the desired position is achieved by first measuring the peri-implant soft tissue thickness from the implant platform to the free gingival margin, then selecting an abutment with a suitable collar height that can be shorter than the soft tissue thickness to position the finish line subgingivally or greater than the soft tissue thickness to position the finish line supragingivally. It is therefore important to give the soft tissue a chance to heal and stabilize after second-stage surgery to be able to properly locate the restoration finish line [21] (Fig.  8.16). Measuring peri-implant soft tissue thickness can be performed by using many instruments, the easiest of which is a plastic periodontal probe (Fig. 8.17).

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a

b

Fig. 8.15 (a) Cement retention provides passivity with multiunit restorations, especially when abutments are parallel. (b) Screw access channels in favorable positions not interfering with the esthetic or biomechanical properties of the restoration

Cement-retained restorations have always been guilty of causing peri-implant soft tissue irritation and inflammation due to the excess cement that is difficult to completely remove. The main cause of peri-implant soft tissue problems associated with cement-retained restorations is the inappropriate finish line location resulting

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Fig. 8.16  Soft tissue healing following second-stage surgery

Fig. 8.17 Measuring peri-implant soft tissue thickness by using a plastic periodontal probe

from improper abutment collar height selection or designing. A cement-retained restoration with a supragingival finish line does not cause any soft tissue problems as excess cement can be completely removed. Even if a 1 mm subgingival finish line is used, excess cement can still be removed conveniently. However, in the case of deep subgingival finish lines greater than 2 mm, excess cement removal becomes very difficult, especially interproximally, as it is associated with bleeding and pain preventing proper cement removal. Residual cement causes peri-implant soft tissue problems that can advance to peri-implantitis [2] (Fig. 8.18).

8.1.3.3 Relation Between Finish Line Contour and Peri-implant Soft Tissue Contour Measuring peri-implant soft tissue thickness is usually performed at the midfacial region. However, peri-implant soft tissue thickness may vary between the midfacial and interproximal regions. The difference would be less in cases associated with loss of interdental papillae and more in cases with well-preserved interdental papillae (Fig. 8.19a,b).

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Fig. 8.18  Excess cement associated with a deep subgingival finish line

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b

Fig. 8.19 (a) Flat peri-implant soft tissue margin associated with loss of interdental papillae. (b) Curved peri-implant soft tissue margin associated with well-preserved interdental papillae

Stock abutments usually have a finish line that has a straight contour. To achieve a 1-mm subgingival finish line position, the abutment collar height should be 1 mm shorter than the peri-implant mucosa thickness at the midfacial region. The problem usually exists at the proximal surfaces, where the 1-mm subgingival midfacial finish line becomes much deeper interproximally due to the thicker peri-implant mucosa at the interdental papilla region (Fig. 8.20a,b). When cement-retained restorations are used over stock abutments with a 1-mm subgingival midfacial finish line, excess cement would be easily removed facially but would be very difficult to remove interproximally. In such cases, custom-made cement-retained abutments are preferred and recommended [22, 23] (Fig. 8.21). Stock abutments can be acceptably used in cases with missing interdental papillae where the soft tissue contour is flat rather than curved (Fig. 8.16). Custom-made abutments can be constructed by using conventional techniques or CAD-CAM technology. They can have a custom-made emergence profile together with a finish line contour that matches the peri-implant soft tissue contour. A 1-mm subgingival finish line can be maintained all around the restoration margins, making excess cement removal feasible and predictable (Fig. 8.21). Screw-retained restorations are often preferred over cement-retained ones from a peri-implant soft tissue health point of view. Excess cement, when not completely removed, has always been a frequent reason for peri-implant soft and hard tissue

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b

Fig. 8.20 (a) Peri-implant soft tissue thickness at the midfacial region is much less than at the interproximal region. (b) When using stock abutments with a flat finish line contour, excess cement would be very difficult to remove due to the thick interproximal soft tissue, making the finish line deep subgingivally Fig. 8.21 Custom-made cement-retained abutments can have a finish line that follows the peri-implant soft tissue margin making excess cement removal more predictable

problems [2]. However, a big part of the problem is related to the location of the abutment restoration finish line. Properly constructed cement-retained restorations with proper finish line location can be as good as screw-retained ones.

8.2 Prosthetic Materials and Their Relation to Peri-implant Soft Tissue Health The increasing demand for esthetic restorations has triggered the advancement and improvement of tooth-colored materials to match the high biomechanical and esthetic expectations. Tooth-colored materials are usually nonmetallic, either ceramic based or polymer based. However, metals are still being used with specific

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indications mainly related to their biomechanical superiority. Commonly used materials include metals such as gold, titanium, and cobalt chromium. Nonmetallic materials include ceramics, zirconia, resin nano ceramics, and BioHPP.  Acrylics can also be used, however, mainly as temporary restorative materials [24, 25]. Implant restorations can be constructed by using conventional techniques or CAD-CAM technology that is taking over prosthodontics to a new dimension. All prosthetic materials are currently being produced for CAD-CAM fabrication, which has improved the accuracy and reduced the time needed for prosthesis construction. Improving the accuracy involves reducing the micro gap between prosthetic components that in turn improves the peri-implant soft tissue health and reduces complications. The selection of prosthetic materials is usually based on many factors, including biomechanical, esthetic, and biological. Despite the importance of the biomechanical and esthetic features and properties of restorative materials, their biological interaction with peri-implant soft tissues is of major importance. In many situations, the prosthetic material becomes in direct contact with peri-implant soft tissues, especially with subgingival finish lines (Fig. 8.22). Polished metals especially titanium have produced acceptable results [26, 27]. Glazed ceramic has also shown good soft tissue response [28]. Acrylics are used with caution as they are porous and therefore less hygienic than other definitive materials. They are also stained easily and therefore need to be changed frequently. When acrylic is included in a definitive implant restoration, it is always advisable to fabricate the restoration screw retained [3]. Many studies were conducted to evaluate the peri-implant soft tissue response to different prosthetic materials [29]. Brunot-Gohin et al. [30] investigated soft tissue

Fig. 8.22  With subgingival finish lines, restorative material becomes in direct contact with peri-­ implant soft tissues

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Fig. 8.23  Lithium disilicate restorative material. Can be polished or glazed

response to lithium disilicate with three different surface treatments: raw surface treatment, hand-polished surface treatment, and glazed surface treatment. Lithium disilicate polished ceramic provided better adhesion and proliferation than lithium disilicate glazed ceramic (Fig.  8.23). Van Brakel et  al. [31] compared the peri-­ implant soft tissue response to titanium versus zirconia abutments. No differences in soft tissue health were seen in peri-implant mucosa adjacent to zirconia and titanium abutment surfaces. Similar results were demonstrated in an animal study by Blanco et  al. [32], where peri-implant soft tissue response to implant abutments made of zirconia and titanium was similar after 9 months of healing.

8.2.1 CAD-CAM Technology CAD-CAM technology has revolutionized prosthodontics. Digital workflows have replaced conventional procedures in almost all prosthetic work. The reason for that is that CAD-CAM technology improved the accuracy and predictability of prosthetic restorations and reduced the time and steps needed to fabricate restorations [23, 27, 33, 34]. The impact of CAD-CAM technology on peri-implant tissues is related to acquisition procedures together with marginal accuracy and passivity of restorations. Acquisition procedures involve digital impressions obtained by using scan bodies attached to implants or abutments [27, 34, 35]. When properly seated, scan bodies lightly retract peri-implant soft tissues, eliminating the need for soft tissue retraction associated with conventional impressions (Fig. 8.24). Restorations performed by using CAD-CAM technology are machine dependent, eliminating the personal variation associated with dental technicians. Restoration margins and passivity are therefore more predictable with their positive impact on peri-implant soft and hard tissues [33, 36] (Fig. 8.25a,b).

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Fig. 8.24  Scan bodies lightly retract peri-implant soft tissues, eliminating the need to use a retraction cord

Fig. 8.25  CAD-CAM fabricated restorations have a precise marginal adaptation

8.2.2 Anodic Oxidation of Titanium Abutments Titanium abutments have been used successfully over dental implants for many years. Peri-implant soft tissue response to polished titanium abutment collars has shown favorable results [37]. Their main drawback is their unesthetic color especially when used in the esthetic zone in cases with thin gingival biotype. Several attempts have been made to change the abutment color by using different materials and coatings. Gold, metal-ceramic, nitride-treated titanium, composite resin-coated

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titanium, thermal oxidation, chemical oxidation, and anodic-oxidized titanium have been used to mask the unesthetic grayish abutment color, especially the abutment collar [26, 38–43] (Fig. 8.26). Anodic oxidation is a surface modification technique for changing the abutment color. Titanium is spontaneously coated with an oxide surface layer as soon as it is exposed to atmospheric air. Anodic oxidation promotes the production of a thick oxide surface layer based on the voltage used. Specific colors can be produced by controlling the variation in oxide layer thickness that interacts differently with light [44]. Studies have been conducted to evaluate the esthetic outcome of anodically oxidizing titanium abutment collars. Pink collars have been shown to improve gingival esthetics by masking the grayish titanium color [26, 43, 45] (Fig.  8.27a,b). In Fig. 8.26 Anodically oxidized abutment collar. The pink color masks the unesthetic grayish abutment color

Fig. 8.27  Anodically oxidized pink abutment collar

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addition, anodic oxidation alters the surface characteristics of titanium. Increasing the thickness of the surface oxide layer has also been reported to improve its surface hardness and corrosion resistance [46]. In an in vitro study, Wang et al. [45] reported that anodization increased the grain formation, surface roughness, and hydrophilicity of titanium. Although smooth machined titanium surfaces have been recommended for their improved soft tissue response, a degree of roughness is desirable. While the optimal degree of roughness is unclear, the proliferation of human gingival fibroblasts, their viability, and cell morphology have been reported to be similar on anodized and unanodized surfaces. In a split-mouth study, Farrag and Khamis [44] investigated the effect of anodized titanium on peri-implant soft tissue health and esthetics. Pink anodized titanium abutment collars did not produce a clinically significant effect on the health of peri-­ implant soft tissues. Anodic oxidation of titanium abutment collars is therefore an effective method to mask their grayish unesthetic color, especially in cases with thin gingival biotypes, without clinically compromising peri-implant soft tissues.

8.3 Prosthetic Complications with a Biological Impact Achieving patient satisfaction is always the ultimate goal. However, complications and even implant failure are possible. Implant failure is not something that happens overnight. Failure is usually preceded by a complication that, if not recognized and properly handled, will eventually propagate to failure. Complications can happen in every step of implant treatment if the procedure is not performed in a correct manner. Problems can result from improper patient selection, which involves prosthetic and surgical considerations, psychological evaluation, and even financial considerations. Complications can occur during implant placement, during the healing period, during the prosthetic procedures, and later on after months and years of use. They can also be related to the soft tissue, bone, or the prosthesis itself. Prosthetic complications with a biological impact on peri-implant bone and soft tissue include restorations with open contacts or margins, improper occlusion, cantilevers that are too long, screw loosening, non-passive restorations, and connecting implants to natural teeth. Restorations with open contacts result in food impaction, causing peri-implant soft tissue inflammation known as peri-implant mucositis [47–49]. If not properly treated, it can propagate to peri-implantitis (Fig. 8.28a–c). Restorations with open margins or micro gaps at the implant abutment or abutment restoration interfaces can also harbor food and bacteria, resulting in soft tissue problems and later on bone loss, especially if the restoration margins or micro gaps are subgingival (Fig. 8.29). Restorations that are not passive, or those with too long cantilevers, or improper occlusion in the form of high points, deflective occlusal contacts, or restorations with sharp cusps can cause undue stress transmitted to the bone, causing bone

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a

b

c

Fig. 8.28 (a) Food impaction distal to the implant due to an open contact. (b) Bone level on the day of restoration insertion. (c) Bone loss on the distal side of the implant resulting from food impaction

resorption that is usually associated with implant surface exposure causing soft tissue problems [6] (Fig. 8.30a,b). Abutment screw loosening is a frequent complication. Reasons include improper screw torquing according to the manufacturer’s instructions, non-passive restorations, improper occlusion, and inaccurate fit between implant components [2]. Screw loosening is associated with biomechanical problems together with micro gaps causing food accumulation that ends up with soft tissue problems [50]. Restoration and abutment micro movement and later on macro movement can also cause mechanical irritation to peri-implant soft tissues with resultant problems (Fig. 8.31). Connecting implants to natural teeth is a debatable issue. Movement of natural teeth due to the compressibility of the periodontal ligament results in undue stresses transmitted to implants, causing peri-implant bone loss and later on soft tissue problems (Figs.  8.32,8.33). Most of the studies advocate not connecting implants to natural teeth except in very limited conditions when it is absolutely necessary to avoid biomechanical and biological problems [51, 52].

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Fig. 8.29  Restorations with an open margin can result in soft tissue problems. Peri-implant mucositis resulting from a restoration with open margins

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b

Fig. 8.30 (a) Un-passive restoration with an open margin resulting in bone loss associated with the distal implant. (b) Improper occlusion resulting in crater-like bone resorption

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Fig. 8.31  Abutment screw loosening can be detected on an X-ray by the presence of a micro gap between the implant and abutment

Fig. 8.32 Connecting implants to natural teeth results in bone loss around implants

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b

Fig. 8.33 (a) Natural tooth caries resulting in a long cantilever on the implants with evident bone loss related mainly to the distal implant. (b) Carious tooth totally separated from the bridge

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38. Ishikawa-Nagai S, Da Silva J, Weber H, Park S. Optical phenomenon of periimplant soft tissue. Part II. Preferred implant neck color to improve soft tissue esthetics. Clin Oral Implants Res. 2007;18:575–80. 39. Abrahamsson I, Berglundh T, Glantz PO, Lindhe J. The mucosal attachment at different abutments: an experimental study in dogs. J Clin Periodontol. 1998;25:721–7. 40. Lim H-P, Lee K-M, Koh Y-I, Park S-W.  Allergic contact stomatitis caused by a titanium nitride-coated implant abutment: a clinical report. J Prosthet Dent. 2012;108:209–13. 41. Jung RE, et  al. In vitro color changes of soft tissues caused by restorative materials. Int J Periodontics Restorative Dent. 2007;27(3):251–7. 42. Jung RE, et  al. The effect of all-ceramic and porcelain-fused-to-metal restorations on marginal peri-implant soft tissue color: a randomized controlled clinical trial. Int J Periodontics Restorative Dent. 2008;28(4):357–65. 43. Tu Z, Zhu Y, Li N, Hu H, Cao L. Applications and advances on surface treatment for titanium and titanium alloy. Surf Tech. 2009;38:76–7. 44. Farrag KM, Khamis MM. Effect of anodized abutment collars on peri-implant soft tissue: a split-mouth clinical study. J Prosthet Dent. 2021;130:59–67. 45. Wang T, Wang L, Lu Q, Fan Z. Changes in the esthetic, physical, and biological properties of a titanium alloy abutment treated by anodic oxidation. J Prosthet Dent. 2019;121:156–65. 46. Charrière R, Lacaille G, Pedeferri MP, Faucheu J, Delafosse D. Characterization of the gonioapparent character of colored anodized titanium surfaces. Color Res Appl. 2015;40:483–90. 47. Zitzmann NU, Berglundh T.  Definition and prevalence of peri-implant diseases. J Clin Periodontol. 2008;35(8 Suppl):286–91. https://doi.org/10.1111/j.1600-­051X.2008.01274.x. 48. Roos-Jansåker AM, Lindahl C, Renvert H, Renvert S.  Nine- to fourteen-year followup of implant treatment. Part II: presence of peri-implant lesions. J Clin Periodontol. ­ 2006;33(4):290–5. https://doi.org/10.1111/j.1600-­051X.2006.00906.x. 49. Derks J, Tomasi C. Peri-implant health and disease. A systematic review of current epidemiology. J Clin Periodontol. 2015;42(Suppl 16):S158–71. https://doi.org/10.1111/jcpe.12334. 50. Huang Y, Wang J.  Mechanism of and factors associated with the loosening of the implant abutment screw: a review. J Esthet Restor Dent. 2019;31(4):338–45. https://doi.org/10.1111/ jerd.12494. Epub 2019 May 31. 51. Misch C, Ismail Y. Finite element stress analysis of tooth-implant fixed partial denture designs. J Prosthet Dent. 1993;2:83–92. 52. Chee W, Jivraj S. Connecting implants to teeth. Br Dent J. 2006;201(10):629.

9

Occlusion and Peri-implant Soft Tissues Mohamed Hassan

9.1 Effects of Occlusion on Soft Tissues Around Dental Implants In order to properly apply occlusal concepts, it should not be dealt with only as how teeth come in contact, whether in static or dynamic occlusion; rather, it is recommended to perform occlusal evaluation and analysis and incorporate it into the comprehensive oral evaluation. This evaluation should include both physiologic functions and nonphysiologic functions. Dental occlusion is controlled by the dynamic process of mastication, which is regulated by the elements of the masticatory system. The occlusal forces applied during teeth contact can either be within the adaptive capacity of the masticatory system or it may exceed the adaptive limit in which case it will cause destruction to the system. The ability of the system to withstand different levels of forces may vary from one individual to another and may also change from time to time on the same person. When the adaptive capacity is less than the applied forces, the resultant injury to the tissues is called trauma from occlusion [1–3]. Traumatic occlusion relates to its destructive effects and not necessarily how teeth occlude. Trauma from occlusion can either be primary or secondary; primary trauma from occlusion is a result of alterations of occlusal forces. When the manifestation of traumatic occlusion results from the reduced ability of the tissues of the masticatory system to resist the forces, it is then considered secondary trauma from occlusion [4].

M. Hassan (*) Oral Medicine, Infection & Immunity, Harvard school of dental medicine, Boston, MA, USA e-mail: [email protected] © Springer Nature Switzerland AG 2023 M. Hassan (ed.), Peri-Implant Soft Tissue Management, https://doi.org/10.1007/978-3-031-45516-2_9

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Traumatic occlusion can also be either acute or chronic; acute trauma from occlusion is in the case of biting on a hard object, which will result in pain and sensitivity and or tooth movement. Chronic trauma from occlusion is more common to take place gradually and causes more destruction than acute trauma from occlusion. Even though parafunction habits, as an example of chronic trauma from occlusion, are very common and affect a wide range of populations, they are still challenging to diagnose and manage. In this chapter, bruxism will be discussed in more detail as the most common parafunctional activity to give dental practitioners an overview of its effects on the masticatory system, including soft tissues around natural teeth as well as dental implants. The process of mastication is complex because it combines the elements of the masticatory system, or the teeth, periodontium, temporomandibular joints, and the muscles of mastication. The masticatory system is designed to function properly under the normal physiological limits of forces that occur during functional activities. Functional activities involve movements of the face, talking, yawning, brushing the teeth, shaving, washing the face, turning the head, stooping over, and the effects of swallowing, head position, and body position. The complete oral evaluation must consider the difference in effect between functional activities and parafunctional activities, such as bruxism, clenching, tapping, and nail biting [5]. Based on the studies of functional occlusal forces by Glickman et al., Haddad et al., and Graf and Mehta et al., it has been shown that “the forces of mastication are of minimal duration and intensity and as such are unlikely to cause the type of occlusal breakdown seen in patients” [6]. The amount of force applied by parafunctional activities is as much as four times as those during functional activities [7]. Forces that exceed the physiological limit could be destructive to one or more elements of the masticatory system. This destruction may further lead to complications, such as systemic or intra-oral manifestations, as in the case of parafunctional activities. Parafunctional activities have been etiological factors in occlusal breakdown. Further understanding is needed regarding the effect that occlusal interferences have on teeth, periodontium, and jaw function. In cases of occlusal disharmony, experiments have detected that maximum intercuspation may harm the periodontal ligament and pulpal tissues of the affected tooth. In addition, this may disrupt smooth jaw function and may cause jaw muscle pain, clicking, and other symptoms of TMD [8]. As the literature widely supports, bruxism and its effects are the most prevalent and destructive dental disorders. Although widespread, even in its late stages, it is often difficult to identify. Studies estimate that bruxism affects as many as 50% of children and 90% of adults [9]. The effects of bruxism are multiple and diverse and may include temporomandibular joint pain and dysfunction [10–16], head and neck pain, tooth wear [13, 17–19], mobility [12, 13], erosion, abrasion, loss of and damage to supporting structures, loss of vertical dimension [20], muscle pain and spasm [13, 14, 19], disturbance of esthetics, behavioral alteration [17], and oral discomfort. The prevalence of bruxism may also lead to widespread and unspecified effects on the masticatory system. Even though it is known that parafunctional activities are more destructive to the masticatory system than functional movements, it is

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uncertain on which masticatory system element the excess force will manifest itself. Just as when the human body falls, a limb “breaks” the fall, the initial “break” to the masticatory system serves as the body’s adaptive mechanism to the increased occlusal forces. Mehta has reported a concept called the Weak Link Theory, which suggests that “when occlusal forces are of such intensity and duration that they override the body’s adaptive capacity, stomatognathic breakdown will occur. If one considers the stomatognathic system as a chain … the weakest link in the chain will ‘break’ first” [21]. If the break manifests itself on the soft tissues around the implants, it may show some signs of deformities such as recession.

9.1.1 Definition of Occlusion It is controversial between authors and clinicians in a wide range, some suggesting it is a tooth-related position [22], while others believe it is a muscles-related position [23]. Still, there is another opinion suggesting it is mainly controlled and related to the temporomandibular joint [24, 25]. Maybe it could also be attributed to a combination between all the masticatory system elements’ function and physiology. The periodontal ligament has some cells distributed and located throughout the periodontal fibers; these cells are called mechanoreceptors and are connected to the neural connection. Mechanoreceptors have been involved in the jaw reflexes and will affect muscles’ functions and how teeth are occluding [26]. When patients become either partially or completely edentulous, the periodontal ligament will disappear after tooth/teeth extraction. With the loss of the periodontal ligament comes the loss of the ligament-impeded mechanoreceptors and their effects on the jaw reflexes and associated muscles. Some studies suggested that even after the teeth loss, some mechanical stimuli still can excite neurons with receptors situated some distance from the periodontium [27]. Dental implants also lack periodontal ligament, and they rather integrate into the bone directly to form bone–implant interface. This type of attachment gives the desired osteointegration to provide stability to the dental implants. Accompanied with proper function and acceptable esthetic results to both patients and dental providers, dental implants can then be considered successful. Failure of dental implants can either take place before loading the implants with the proper restoration in which case it can be related mainly to the surgical phase. Meanwhile, if the implants fail after loading them, then it is reasonable to think that occlusion may play a role in that failure, especially in case overloading exists.

9.1.2 Effects of Traumatic Occlusion on Dental Supporting Tissues Occlusal trauma can cause different levels of tissue reaction in both natural teeth and implants. Based on the adaptive capacity of the tissues, the excessive forces

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may cause some damage with different levels to one or more than one of the elements of the periodontium. The periodontal ligament is always under constant remodeling as a response to increased occlusal forces. In most cases, after the elimination of the excessive forces, the ligament is capable of readapting to reverse the damaging effects of the excessive forces. In the absence of inflammation, excessive occlusal forces are unable to manifest significant changes in probing depth, bone loss, and bone–implant contact compared to non-loaded healthy implants in dogs [28]. On the other hand, when implants placed in monkeys had regular plaque control measures, it resulted in the loss of osteointegration, as shown in the histologic changes in rats [29]. In order to understand the mechanism of remodeling, tissue response can be understood as happening in three stages. These stages are injury, repair, and adaptive mechanism [30, 31]. It is important to note that after teeth extraction, regardless of the replacement option, tissue change is expected in the socket in the 12 months after tooth loss. The estimated loss is about 50%, which is about 5–7 mm, about two-thirds of that loss occurs in the first 3 months [32]. These changes happened on both hard and soft tissues and in both vertical and horizontal dimensions [33].

9.1.3 Bruxism and Dental Implants Placing dental implants in patients exhibiting bruxism manifestations has been mentioned in multiple studies and clinical trials; some authors believe bruxism should be considered as a contraindication for dental implants [34]. However, other studies found that despite the negative effects of bruxism on dental implants, it is still not conclusive that bruxers should not have implants as an option for missing teeth replacement due to the irritability of the studies due to the limited number of subjects [35]. Different complications were documented on dental implants due to occlusal overload as a result of bruxism; these complications, such as fracture of implants, fracture of ceramic or porcelain, screw loosing, or fracture, will lead to implant failure [36]. PDL around natural teeth helps in absorbing and distributing occlusal load produced during tooth contact and masticatory function via the alveolar bone proper [37]. Meffert has indicated that the greater the magnitude of forces applied to dental implants, the greater the difference between the implant and the bone interface. This will lead to fibrous tissue ingrowth to accommodate the difference between the implant and the bone surface [38].

9.1.4 Definition and Physiopathology of Bruxism Bruxism is a mandibular parafunction that includes forcible clenching, tapping, or grinding of the teeth [39]. Bruxism is a centrally induced phenomenon that is common to all people and unrelated to surface factors [40]. The movement is often rhythmic in nature and may have a physiological or neurological basis. The grinding

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episodes may be a form of autonomic reflex [41]. Parafunctional behaviors differ from normal functional activities in that they are often unconscious; it is common for patients to deny or be unaware of such habits [7]. Parafunctional activities may occur diurnally or nocturnally. Diurnal bruxism is thought to be a learned behavior, while nocturnal bruxism is considered to be related to stress [42, 43]. More studies focus on nocturnal parafunction because it is suggested that muscular dynamics during sleep exert a greater mechanical load on the temporomandibular joints than do those that occur during diurnal clenching [39, 44]. Forces applied during nocturnal parafunction can exceed four times that of normal function, such as eating and swallowing [45]. Furthermore, the American Sleep Disorders Association (ASDA) [46] suggested that the use of “nocturnal” should be replaced by “sleep” bruxism in order to include the activities that can occur during daytime sleep. Bruxism has been noted during most stages of sleep, but it occurs predominantly during stage 2 (non-REM) and REM sleep. It rarely occurs during stage 3 and stage 4 sleep. “Bruxing events occur frequently when going from a deeper to lighter stage of sleep, perhaps as an arousal mechanism. Both the frequency and severity of bruxism vary from night to night and appear to be closely associated with emotional and physical stress” [47]. Bruxism affects a wide range of the population. It is estimated to affect 50% of children and as many as 96% of adults, both male and female [9]. Solberg and colleagues estimate the amount of parafunctional activity for two non-patient populations to be 41%, while the signs and symptoms of bruxism in a study population to be between 80–90% [45]. Most adults and children indulge in nocturnal bruxing activities to a varying degree at some point in their lives [48]. While bruxism affects a large percentage of the population, some populations may be more likely to exhibit signs of bruxism. These populations may exhibit risk factors that include certain personality types, gender, and age [49]. Female patients report more clenching, but no sex differences have been noted [46, 50–52]. In addition, the highest prevalence of bruxism is noted for the 20–50-year-old age group [51, 52], and its frequency decreases with age [48, 53]. Patients who exhibit mouth breathing and sleep apnea also may have nocturnal bruxism [47].

9.1.5 Etiology of Bruxism Many etiological factors have been suggested to cause sleep bruxism, but there are still limited conclusive findings about its etiology. Most identify mental conditions or stress. Nocturnal bruxism is generally believed to be a stress-related sleep disorder [9, 43, 54]. Additional possible causal factors include occlusal disorders, allergies, and sleep positioning [9]. Another speculated cause for nocturnal bruxism is elevated mental and physical alertness [55]. In a cross-sectional study, significant correlations were found between different types of morphologic malocclusion, such as class II and III, and molar relationship, deep bite, over-jet, and tooth wear or grinding. This suggests that malocclusion does not increase the probability of

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bruxism, and therefore early treatment of occlusion to prevent bruxism is not scientifically justified [56]. Because of its nonspecific pathology, bruxism may be difficult to diagnose [9] and is often measured indirectly through sleep patterns, tooth wear, mobility, and muscle pain. Parafunctional habits have been most frequently assessed by indirect means, such as patient’s self-report, questionnaires, reports by bedroom partners, and tooth wear [57]. Because of the insufficient knowledge about the etiology of bruxism, there has been difficulty in diagnosing and managing bruxism. Dentists usually focus on a local cause or treat the damage caused by bruxism. This mismanagement may lead to unnecessary and irreversible dental treatment, with little impact on the incidence of bruxism [58]. As an alternative management to bruxism, some studies are exploring the interaction between nocturnal bruxism and sleep posture. This would assist preventive dentistry by shifting dental treatment from a search for a minimum local dental cause to sleep posture [59].

9.1.6 Management of Bruxism Management of parafunctional habits is a multifaceted procedure that requires dentists to have a sufficient background and knowledge of their etiology and effects. Successful management must treat both the cause of bruxism and its effects. The etiology of bruxism is often undefined, which makes it difficult to treat. In addition, some of the effects of bruxism cannot be reversed, as in tooth structure loss. However, the underlying cause should be managed to avoid further dental, periodontal, and other masticatory system damage [60]. Because bruxism is widely thought to be a stress-related habit, its treatment often includes stress management. For most people, daily life poses numerous causes of stress, many of which cannot be removed and must be managed. Researchers have supported a range of techniques to manage stress, varying from a personality assessment [61] to exercise [62] to hypnotherapy [63–65]. Other attempts to reduce stress include drug therapy [9, 66], stress reduction therapy [9], physical therapy [9], ice therapy, [67] change in sleep position [9], and antidepressants [68]. While the possible approaches to stress reduction are varied and numerous, hypnotherapy and biofeedback are the most frequent treatment recommendations. Patients who reported bruxing activities were monitored with a portable EMG in order to determine baseline bruxing. After suggestive hypnotherapy, self-reports and post-treatment EMG readings evaluated the results of hypnotherapy. Only self-­ reporting patients monitored the long-term effects. As a result of the therapy, bruxers showed a significant decrease in EMG activity and reported less facial pain, and their partners reported less bruxing noise immediately following treatment and for a range of 4–36 months [64]. More intensive hypnotherapy and psychological interventions are still in the early stages of experimentation and verification. A 55-year-old male bruxer who had undergone 10 years of craniomandibular treatment and use of a dental split was

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given a projective hypnoanalytic exploration. The purpose of the hypnosis was to identify and resolve an earlier source of conflict that had become a constant source of mental and muscular tension. The hypnoanalytic exploration was followed by an audio-taped cognitive-behavioral hypnotic intervention and prescribed bedtime practice. Post-therapy psychological, physiological, and self-report measurements corroborated the patient’s sense of well-being and ability to sleep without the dental splint [69]. Because bruxism is a largely unconscious behavior, researchers suggest that raising the patients’ consciousness about their behavior may help reduce it. Bruxism is usually performed in an unconscious manner, and many bruxers are not aware of their own bruxing [70]. Biofeedback treatment may be used separately or in conjunction with another treatment plan. In a study of three subjects, patients were conditioned to be more aware of their bruxing. The first subject was awakened by a loud tone, which she manually reset. The second subject was given relaxation training and biofeedback. While the relaxation training failed to decrease her bruxing, biofeedback successfully decreased the frequency and duration of bruxing episodes [71]. Although bruxism is widely considered to be a stress-related psychosomatic syndrome, there is no definitive information about its cause [9, 43, 54]. Thompson identifies additional possible causal factors that include occlusal disorders, allergies, and sleep positioning. Another speculated cause for nocturnal bruxism is elevated mental and physical alertness [55]. In addition to identifying the etiology of bruxism, successful bruxism management should include identifying and treating the effects of bruxism. Bruxism may lead to damage of the dental apparatus. This damage may indicate the need for restorative treatment [14, 20, 72], orthodontic treatment [72], and occlusal adjustment [72–75]. The clinician who encounters a patient with severe bruxism activities may consider stress but should also do a comprehensive physical and nonphysical analysis of obvious and unapparent issues that may impact the interactive effects of bruxism.

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